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1.  Radiation-associated cardiovascular risks for future deep-space missions 
Journal of Radiation Research  2014;55(Suppl 1):i37-i39.
Background: During the future Moon and Mars missions, astronauts will be exposed to space radiation (IR) for extended time. The majority of space flight-associated risks identified for the cardiovascular (CV) system to date were determined shortly after low Earth orbit (LEO) short- and long-duration space flights that include: serious cardiac dysrhythmias, compromised orthostatic CV response and manifestation of previously asymptomatic CV disease. Further ground-based experiments using a surrogate model of microgravity supported the space flight data for significant cardiac remodeling due to prolonged exposure to microgravity. These symptoms were determined to be a consequence of adaptation to microgravity that could be ameliorated by a post-mission exercise program, and were not identified as risk factors that were causatively related to space IR. Long-term degenerative effects of cosmic IR during and after space flights on CV system are unknown.
It was suggested that due to GCR, each cell in an astronaut's body will be traversed by 1H every 3 days, helium (2He) nuclei every few weeks and high charge and energy (HZE) nuclei (e.g. 28Si, 56Fe) every few months. Despite the fact that only 1% of GCR is composed of ions heavier than helium, ∼41% of the IR dose-equivalent is predicted to be HZE particles with 13% being from 56Fe particles, only. During an exploration-class space mission to Mars, astronauts will not have access to comprehensive healthcare services for a period of at least 2–3 years. Since the majority of experienced astronauts are middle-aged (average age is 46, and the range is 33–58 years), they are at risk for developing serious CV events which could be life-threatening for the astronaut and mission-threatening for NASA. Therefore, it is important to evaluate the effects and potential CV risks caused by space IR. We hypothesized that: (i) low-dose space IR-induced biological responses may be long-lasting and are IR type-dependent; (ii) IR may increase CV risks in the aging heart (IR + AGING model) and affect the heart recovery after an adverse CV event, such as acute myocardial infarct (IR + AGING + AMI model).
Methods: Eight- to 9-month-old C57BL/6N male mice were IR once with proton (1H) 50 cGy, 1 GeV/n or iron (56Fe) 15 cGy, 1 GeV/n. We evaluated IR-induced biological tissue responses—underlying molecular mechanisms, calcium handling, signal transduction, gene expression and cardiac fibrosis. Cardiac function was assessed by echocardiography (ECHO) and hemodynamic measurements (HEMO) as detailed in Fig. 1. AMI was induced by ligation of left anterior descending coronary artery 1 and 3 months post-IR as detailed in Fig. 2.Fig. 1.Radiation + aging model. Fig. 2.Radiation + aging model + adverse CV event model.
Results: In the IR + AGING model, cardiac function was not different among the control and 1H-IR group, whereas left ventricular end-diastolic pressure (LVEDP) was significantly increased in 56Fe mice 1 and 3 months post-IR. There was a small but statistically significant (P < 0.04) improvement of ejection fraction % (EF%) in 1H-IR vs control mice. One month post-IR, compared with control, 1H- and 56Fe-IR hearts had a significant up-regulation of sarcolemmal Na+–Ca2+ exchanger (NCX) (∼200% P<0.007), sarco(endo)plasmic reticulum calcium-ATPase (SERCA2a, >200% increases, P < 0.02) and 400% decreases in p-p38 MAPK (P < 0.05), suggesting activation of compensatory mechanisms in [Ca2+]i handling in these hearts. By 3 months, compared with control, 1H- and 56Fe-IR hearts had 200–500% (P < 0.02) decreases in SERCA2a and more than 200% decreases in p-Creb-1 (P < 0.02), suggesting reduced capacity in intracellular [Ca2+]i handling. These data suggest that dysfunction in [Ca2+]i handling combined with LVEDP increase after 56Fe-IR may arise from the excessive demand on the heart due to prolonged activation of compensatory mechanisms that lead to changes in SERCA2a and p-Creb1 levels. This may represent a possible intracellular mechanism of heart failure in development in 56Fe-IR hearts.
In the IR + AGING + AMI model, no mortality was observed among three different groups 1 or 3 months post-IR and up to 28 days post-AMI. However, 1 month post-IR and 28 days post-AMI, the infarct size was significantly smaller in 56Fe-IR (p < 0.003) and 1H-IR (p = n.s.) vs control-IR mice, suggesting that at 1 month, 56Fe-IR primes the heart to recover better after AMI. In contrast, 3 months post AMI, 1H-AMI mice had a better cardiac functional recovery compared with control-AMI and 56Fe-AMI mice. The ejection fraction (EF%) was most decreased in 56Fe-AMI mice (56Fe-AMI vs 1H-AMI: 18 vs 48%, P < 0.007, ∼65–70% pre-AMI EF% for all groups). There was a 2- to 4-fold increase in LVEDP in 56Fe-AMI vs 1H-AMI (P < 0.04), suggesting that 56Fe-AMI hearts developed cardiac de-compensation. Western blots showed that 3 days post-AMI, compared with control- and 1H-IR-AMI mice, 56Fe-IR-AMI hearts had a 4- to 7-fold (P < 0.04) decreases in p-Akt (Thr308), p-Erk1/2 (P < 0.007) and ∼2-fold (P < 0.01) increase in phosphorylated ribosomal protein S6 kinase (p-S6k, a readout for mTORC1 pathway activation), suggesting decreased survival and angiogenesis signaling and decreased autophagy in these hearts. Seven days post-AMI, the levels of p-pErk1/2 were comparable between all three treatment conditions. However, in 56Fe-IR-AMI hearts, the p-Akt (Thr308) levels remained 4-fold decreased. Additionally, here was a 3-fold (P<0.05) decrease in p-S6k levels and >10-fold increase in p-p38 MAPK level in 56Fe vs control and 1H-IR-AMI hearts, suggesting continuous decreases in the survival, proliferation and angiogenesis signaling (p-Akt and p-S6k) and increase in the apoptotic signaling (p-p38 MAPK) up to Day 7 post-AMI in 56Fe-IR-AMI mice.
In summary, our results revealed that by 1 and 3 months post-IR in IR + AGING, 56Fe-IR but not 1H-IR mice had worse cardiac function. Further, a single 1H-IR 3 months prior to AMI improved, whereas 56Fe-IR worsened, recovery from AMI recovery. Our data in the IR + AGING and IR + AGING + AMI groups strongly suggest that low-dose HZE particle IR (56Fe) have long-lasting negative effect on heart homeostasis during normal aging, and present a significant CV risk for recovery after adverse CV event, such as AMI.
PMCID: PMC3941505
HZE; iron; proton; low-dose; cardiovascular risks; Ca2+
2.  Genetic Predisposition and Cellular Basis for Ischemia-induced ST Segment Changes and Arrhythmias 
Journal of electrocardiology  2007;40(6 Suppl):S26-S29.
Recent reports have highlighted the importance of a family history of sudden death as a risk for ventricular fibrillation in patients experiencing an acute myocardial infarction (AMI), pointing to the possibility of a genetic predisposition. This report briefly reviews two recent studies designed to examine the hypothesis that there is a genetic predisposition to the development of arrhythmias associated with AMI. Ventricular tachycardia and fibrillation (VT/VF) complicating AMI as well as the arrhythmias associated with Brugada syndrome, a genetic disorder linked to SCN5A mutations, have both been linked to phase 2 reentry. Because of these mechanistic similarities in arrhythmogenesis, we examined the contribution of SCN5A mutations to VT/VF complicating AMI in patients developing VF during AMI. A missense mutation in SCN5A was found in a patient who developed an arrhythmic electrical storm during an evolving MI. All VT/VF episodes were associated with ST segment changes and were initiated by short-coupled extrasystoles. The G400A mutation and a H558R polymorphism were on the same allele and functional expression in TSA201 demonstrated a loss of function of sodium channel activity. These results suggest that a subclinical mutation in SCN5A resulting in a loss of function may predispose to life-threatening arrhythmias during acute ischemia. In another cohort of patients who developed long QT intervals and Torsade de Pointes (TdP) arrhythmias in days 2–11 following an AMI, a genetic screen of all long QT genes was performed. Six of eight patients (75%) in this group displayed the same polymorphism in KCNH2, which encodes the α subunit of the rapidly activating delayed rectifier potassium current, IKr. The K897T polymorphism was detected in only 3 of 14 patients with uncomplicated myocardial infarction (MI) and has been detected in 33% of the Caucasian population. Expression of this polymorphism has previously been shown to cause a loss of function in HERG current consistent with the long QT phenotype. These observations suggest a genetic predisposition to the development of long QT intervals and TdP in the days following an AMI. These preliminary studies provide support for the hypothesis that there is a genetic predisposition to the type and severity of arrhythmias that develop during and after an acute myocardial infarction and that additional studies are warranted.
PMCID: PMC2121617  PMID: 17993325
Ventricular tachycardia; fibrillation; arrhythmia; ischemia; sudden cardiac death
3.  Cardiotoxicity after massive amantadine overdose 
Journal of Medical Toxicology  2008;4(3):173-179.
Amantadine hydrochloride is an antiviral medication used as therapy for parkinsonism and as a cognitive enhancer. We report 2 cases of massive, acute ingestion of amantadine hydrochloride confirmed with serial serum levels.
Case Reports
A 47-year-old woman presented to the emergency department (ED) 30 minutes after ingesting 10 g of amantadine (150 mg/kg) by her report. Initial ECG revealed a sinus rhythm with rate of 93 bpm, and a QRS of 84 msec. While in the ED, the patient sustained a pulseless cardiac arrest and the monitor revealed ventricular tachycardia. She was successfully defibrillated. Postdefibrillation ECG showed a sinus rhythm (rate = 82 bpm), QRS of 236 msec, and QTc of 567 msec. The serum potassium was 1.0 mEq/L (1.0 mmol/L). The patient was given 300 ml (300 cc) 3% sodium chloride IV over 10 minutes. Ten minutes after completion of the hypertonic saline infusion, the patient’s ECG abnormalities resolved and the QRS was 88 msec. Her potassium was repleted over the next 11 hours postpresentation, and she also received an IV bolus of 4 g of magnesium sulfate immediately after the cardiac arrest. No further hypotension, dysrhythmia, conduction delay, or ectopy was noted during the patient’s hospital stay. The second case involved a 33-year-old female patient who presented 1 hour after ingesting 100 tablets of amantadine hydrochloride (100 mg/tab). Initial ECG revealed sinus tachycardia with a QRS of 113 msec, an R wave in lead aVR of 4–5 mm and a QTc of 526 msec. Her serum potassium was 3.0 mEq/L (3.0 mmol/L), her serum calcium was 9.4 mg/dl (2.35 mmol/L), and serum magnesium was 2.1 mg/dl (0.86 mmol/L) on labs drawn at initial presentation. The patient was intubated for airway protection, and her potassium was repleted and corrected over the next 9 hours. Her ECG abnormalities improved 8 hours after initial presentation and normalized at approximately 14 hours postingestion. The patient was discharged home 11 days after her ingestion.
Acute amantadine toxicity manifests with life-threatening cardiotoxicity. Concurrent, often profound, hypokalemia may complicate the administration of sodium bicarbonate in the management of cardiac dysrhythmias.
PMCID: PMC3550039  PMID: 18821491
amantadine; overdose; torsades; hypokalemia
4.  Effect of spironolactone on cardiac remodeling after acute myocardial infarction 
Few studies have reported the effect of aldosterone receptor antagonist (ARA) on myocardial remodeling after acute myocardial infarction (AMI). This study was undertaken to investigate the preventive effect of ARA on myocardial remodeling after AMI.
A total of 616 patients who had been admitted into the CCU of the First Affiliated Hospital of Harbin Medical University from January 2008 to January 2010 were studied prospectively. Only 528 patients were observed completely, including 266 of the control group and 262 of the treatment group. There was no statistical difference in age, gender, medical history, admission situation, and treatment between the two groups (P>0.05). The preventive effects of spironolactone on cardiac remodeling, left ventricular function, renal function and blood levels of potassium were evaluated by echocardiography, serum potassium and serum creatinine at one-month and one-year follow-up.
The echocardiography indicators such as LVESD, LVEDD, LVEF, LAD-ML and LAD-SI were significantly improved in the treatment group compared with the control group at one year (P<0.05). In the treatment group, LVESD, LVEDD, LVPWT, LVEF, LAD-ML and LAD-SI were more significantly improved at one year than one month (P<0.05, P=0.007 to LVEF), and in the control group LVEF was more significantly improved at one year than one month (P=0.0277). There were no significant differences in serum potassium and serum creatinine levels between the two groups.
On the basis of conventional treatment, the early combination of low-dose spironolactone (20 mg/d) could inhibit cardiac remodeling at late stage and prevent heart failure.
PMCID: PMC4129890  PMID: 25215092
Myocardial infarction; acute; Ventricular remodeling; Atrial remodeling; Aldosterone; Aldosterone blockade; Spironolactone; Cardiac function; Prognosis
5.  Relation between infarct size and ventricular arrhythmia. 
British Heart Journal  1975;37(11):1169-1175.
In order to determine whether ventricular arrhythmia is quantitatively related to infarct size estimated enzymatically we studied 31 patients with acute myocardial infarction without cargiogenic shock. Infarct size index was estimated from hourly serum creatine kinase (CK) changes during periods of 48 to 72 hours. Ventricular arrhythmia was quantified by automated analysis of continuous electrocardiographic recordings over a period of 20 hours with the use of the Argus/H computer system. Patients were classified into three groups according to infarct size index. Patients in all groups had similar average heart rate, blood pressure, serum potassium, and arterial pH and PCO2 values during the first 10 hours after admission. The total number of ventricular ectopic beats (VEB), frequency of couplets, and ventricular tachycardia, and peak rate of ventricular ectopic beats during the first 10 hours after admission were all related to infarct size index. For example, patients with small, medium, and large estimated infarct size averaged 26, 104, and 405 ventricular ectopic beats, respectively. These results suggest that the severity of ventricular arrhythmia early after myocardial infarction is related to the extent of myocardial injury as estimated enzymatically. Thus the apparent efficacy and therefore the evaluation of antiarrhythmic agents early after myocardial infarction may be influenced by the magnitude of injury sustained by the heart.
PMCID: PMC482935  PMID: 53056
6.  Ejection Fraction and Mortality Rate of Patients with Isolated Acute Inferior Myocardial Infarction Reperfused by Streptokinase 
ARYA Atherosclerosis  2011;7(2):54-57.
This study aimed to evaluate the effects of streptokinase on left ventricular ejection fraction and mortality rate of patients with inferior acute myocardial infarction (AMI) without right ventricular myocardial infarction (RVMI).
Fifty five consecutive patients with the diagnosis of inferior AMI without RVMI in the coronary care unit (CCU) of Shariati Hospital in Isfahan were selected for this study. Patients who had a history and/or electrocardiogram (ECG) evidence of previous myocardial infarction, evidence of bundle branch block, historical or clinical findings of valvular or other non-coronary heart diseases or heart failure were excluded. Participants were divided into two groups. Group one (n=28) had no contraindication for taking thrombolytic therapy and group two (n=27) had at least one contraindication for this treatment. Patients in group one took 1,000,000 units streptokinase for one hour. Three days later, LVEF of all participants was measured by an experienced cardiologist using 2-dimentiona1 echocardiography. Patients were followed up until four weeks to assess the mortality rate.
One death in the first 24 hours was reported in group one. However, no death was reported in any group until four weeks after discharge. There was no significant difference in mortality rate during the first 24 hours and four weeks after discharge between the two groups. Mean LVEF in the two groups did not show any significant difference (P=0.21).
Probably streptokinase has no effects on one-month mortality rate and LVEF in patients with inferior AMI without RVMI. Therefore, streptokinase side effects must be taken into consideration when being administered for this group of patients.
PMCID: PMC3347851  PMID: 22577446
Inferior Acute Myocardial Infarction; Left Ventricular Ejection Fraction; Streptokinase; Mortality Rate
7.  Effects of different LAD-blocked sites on the development of acute myocardial infarction and malignant arrhythmia in a swine model 
Journal of Thoracic Disease  2014;6(9):1271-1277.
To explore the effects of various left anterior descending (LAD) artery-blocked sites on the development of acute myocardial infarction (AMI) and malignant arrhythmia in a swine model.
Twenty-two pigs underwent occlusion of the coronary artery with balloon angioplasty were randomly divided into three groups according to the blocked site of the balloon: middle-site-blocked LAD group, bottom-third-blocked LAD group and control group. Then, the development of AMI and malignant arrhythmia, including ventricular tachycardia and ventricular fibrillation during the process of model creation, were recorded. Changes of the hemodynamics, blood gas analysis, electrocardiography, and myocardial enzymes were analyzed in each group before and after occlusion.
Middle-site-LAD blockage resulted in a larger infarction size and the corresponding incidence of ventricular fibrillation was significantly higher than that of the bottom-third-blocked group (P<0.05). After the occlusion, the QTc interval of the Middle-site-blocked LAD group was significantly longer than that in the other groups (P<0.01). Moreover, mean arterial blood pressure (MAP), left ventricular ejection fraction (LVEF), and partial pressure of oxygen (PaO2) were significantly lower, but partial pressure of carbon dioxide (PaCO2) increased, in the Middle-site-blocked-LAD group compared with that in the bottom-third-blocked group (P<0.01). Compared with the control group, the two LAD-blocked groups showed significantly higher levels of Mb, CK-MB, LDH, AST and cTnT (P<0.01) four hours after the artery occlusion. However, these indexes were not significantly different between the two LAD-blocked groups (P>0.05).
Location of LAD blockages in swine models may affect the development of AMI and malignant arrhythmia.
PMCID: PMC4178079  PMID: 25276369
Acute myocardial infarction (AMI); malignant arrhythmia; left anterior descending (LAD); swine
8.  Effect of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction in vivo  
Acute myocardial infarction (AMI) is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-α (TNF-α) on ventricular arrhythmias induced by AMI in rats in vivo.
Two hundred and forty male Wistar rats were randomized into a sham-operation group, an AMI group, and a recombinant human tumor necrosis factor receptor:Fc fusion protein(rhTNFR:Fc) group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery (LAD), and there was no ligation but operation in the sham-operation group. The rhTNFR:Fc group was treated with rhTNFR:Fc(10 mg/kg), a TNF-α antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-α among different groups were detected by histochemistry and real-time fluorescent quantitative PCR.
Expression of TNF-α increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR:Fc group. The time-windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR:Fc group showed a lesser expression of TNF-α protein and a lower incidence of ventricular arrhythmias (P<0.05). There was no obvious change in the sham-operation group.
The expression of TNF-α induced by AMI could contribute to the onset of ventricular arrhythmias.
PMCID: PMC4129766  PMID: 25214942
Acute myocardial infarction; Tumor necrosis factor-α; Ventricular arrhythmia; Recombinant human tumor necrosis factor receptor; Fc fusion protein (rhTNFR: Fc)
9.  Time to treatment with thrombolytic therapy: determinants and effect on short-term nonfatal outcomes of acute myocardial infarction 
OBJECTIVES: To characterize the extent of delay in administration of thrombolytic therapy to patients with acute myocardial infarction (AMI) in Canada, to examine patient-specific predictors of such delay and to measure the effect of delay on short-term nonfatal cardiac outcomes. DESIGN: Secondary cohort analysis of data from the first international Global Utilization of Streptokinase and tPA for Occluded Coronary Arteries (GUSTO-I) trial. SETTING: Sixty-three acute care hospitals across Canada. SUBJECTS: All 2898 Canadian patients with an AMI enrolled in GUSTO-I. MAIN OUTCOMES: Time before arrival at a hospital ("symptom-to-door" time) and time from arrival to administration of therapy ("door-to-needle" time) for patients who had an AMI outside of a hospital, in clinically relevant categories; proportions of patients with nonfatal, serious cardiac events, including shock, sustained ventricular tachycardia, ventricular fibrillation and asystole. RESULTS: Of the total number of patients enrolled, records were complete for 2708; 2542 of these patients (93.9%) had an AMI outside of a hospital. These 2542 patients presented a median 81 (interquartile range 50 to 130) minutes after the onset of symptoms, and the median time to treatment in hospital was 85 (interquartile range 61 to 115) minutes. Whereas a greater proportion of Canadian patients than of patients enrolled in GUSTO-I in other countries reached hospital within 2 hours of symptom onset (71.5% v. 61.2%, p < 0.001), a greater proportion of Canadian patients experienced in-hospital treatment delays of more than 1 hour (75.3% v. 57.1%, p < 0.001). In an analysis of all 2708 patients with complete records, both the unadjusted and adjusted odds of nonfatal cardiac events for those treated 4 to 6 hours after symptom onset were significantly higher than for those treated within 2 hours (odds ratio 1.60, 95% confidence interval 1.09 to 2.37). CONCLUSION: After arrival at a hospital, Canadian patients enrolled in GUSTO-I received thrombolytic therapy more slowly than trial enrollees in other countries. Such delays are already known to decrease the rate of short-term survival after AMI. The findings further show that long time to treatment also increases the odds of nonfatal, serious cardiac events. Hospitals and physicians caring for patients with AMI should routinely assess whether and how they can improve door-to-needle times.
PMCID: PMC1232779  PMID: 9054819
10.  Association of Serum Periostin with Cardiac Function and Short-Term Prognosis in Acute Myocardial Infarction Patients 
PLoS ONE  2014;9(2):e88755.
Periostin was proved to play an important role in extra-cellular matrix remodeling after acute myocardial infarction (AMI). Myocardial periostin was markedly up-regulated after AMI and participated in the maladaptive process of cardiac remodeling. However, few researches focused on the circulating periostin and its significance. This study aims to investigate the association of serum periostin level with cardiac function and short-term prognosis in AMI patients.
Methodology/Principal Findings
We totally recruited 50 patients diagnosed as ST-elevation myocardial infarction. Blood samples were taken within 12 hours after the onset of AMI before emergency coronary revascularization procedures. Serum periostin was measured using enzyme-linked immunosorbent assay. All patients received echocardiography examination within one week after hospitalization. Correlations of serum periostin with echocardiography parameters, Killip class and myocardium injury biomarkers (CK-MB/troponin T) were investigated. AMI patients were divided into two groups by serum periostin level (higher/lower periostin group) and followed up for six months. Primary endpoints included cardiovascular mortality, nonfatal stroke/transient ischemic attack, chest pain occurrence and re-hospitalization. Secondary endpoint referred to composite cardiovascular events including all the primary endpoints.
Serum periostin was in negative association with left ventricular ejection fraction (LVEF) (r = −0.472, *p<0.01) and left atrium diameter (LAD) (r = −0.328, *p<0.05). Positive correlation was found between serum periostin level and Killip class (r = 0.395, *p<0.01). There was no association between serum periostin and CK-MB or troponin T (p>0.05). After six months follow up, patients in higher periostin group showed increased composite cardiovascular events (*p<0.05). Patients showed no significant difference in primary endpoints between the two groups.
Serum periostin was in negative correlation with LVEF and LAD, in positive association with Killip class and higher serum periostin level may be predictive for worse short-term disease prognosis indicated as more composite cardiovascular events six months post AMI.
PMCID: PMC3931651  PMID: 24586384
11.  The Impact of Circadian Variation on 12-Month Mortality in Patients With Acute Myocardial Infarction 
Korean Circulation Journal  2010;40(12):616-624.
Background and Objectives
Although circadian variation in the onset of acute myocardial infarction (AMI) has been reported in a number of studies, not much is known about the impact of circadian variation on 12-month mortality. The aim of this study was to investigate the impact of circadian variation on 12-month mortality in patients with AMI.
Subjects and Methods
Eight hundred ninety two patients (mean age 67±12; 66.1% men) with AMI who visited Kyungpook National University Hospital from November 2005 to December 2007 were included in this study. Patients were divided into groups based on four 6-hours intervals: overnight (00:00-05:59); morning (06:00-11:59); afternoon (12:00-17:59) and evening (18:00-23:59).
Kaplan-Meier survival curves showed 12-month mortality rates of 9.6%, 9.1%, 12.1%, and 16.7% in the overnight, morning, afternoon, evening-onset groups, respectively (p=0.012). Compared with the morning-onset AMI group, the serum creatinine levels (p=0.002), frequency of Killip class ≥3 (p=0.004), and prescription rate of diuretics (p=0.011) were significantly higher in the evening-onset AMI group, while the left ventricular ejection fraction (p=0.012) was significantly lower. The proportion of patients who arrived in the emergency room during routine duty hours was significantly lower in evening-onset groups irrespective of the presence or absence of ST-segment elevation (p<0.001). According to univariate analysis, the 12-month mortality rate in the evening group was significantly higher compared to the morning group (hazard ratio 1.998, 95% confidence interval 1.196 to 3.338, p=0.008).
Patients with evening-onset AMI had poorer baseline clinical characteristics, and this might affect the circadian impact on 12-month mortality. Further studies are needed to clarify the role of circadian variation on the long-term outcome of AMI.
PMCID: PMC3025334  PMID: 21267383
Myocardial infarction; Circadian rhythm
12.  A Study of 100 Cases of Arrhythmias in First Week of Acute Myocardial Infarction (AMI) in Gujarat: A High Risk and Previously Undocumented Population 
Aim: To study the incidence of arrhythmias in the first week of Acute Myocardial Infarction (AMI) with respect to type of arrhythmia, age distribution, sex and location of infarctin a patient population from western India and to evaluate its prognostic value and assessment of effect of pharmacotherapy.
Study Design: A prospective clinical study consisting of 100 patients was undertaken to investigate the relationship of arrhythmia with site of AMI, timing, complications and outcome in terms of mortality and morbidity.
Materials and Methods: Hundred consecutive cases of AMI with arrhythmia admitted in ICCU of Sir Sayaji General Hospital, Vadodara were taken in the study.
Results: Among 100 cases, maximum incidence (41%) was found after 6th decade. Incidence of arrhythmias was higher in males (70%) than females (30%). Anterior wall infarcts (69%) were more common than inferior wall (26%). Ventricular Premature Contraction (VPC) (36.23%) was the commonest arrhythmia is anterior wall MI while Complete Heart Block (CHB) (26.92%) was most frequent in inferior wall MI. A large number of arrhythmias were terminated pharmacologically (39%) whereas 13 % of the arrhythmias persisted in spite of treatment.
Conclusion: Hence, in one of the largest study of this kind in a patient population of Western India, we established VPC’s as the most common arrhythmia in AMI patients. Older patients (sixth decade) and males are affected more commonly. Ventricular tachycardia is more fatal in acute inferior wall MI. Pharmacotherapy was successful in a large number of cases.
PMCID: PMC3939588  PMID: 24596724
Arrhythmia; Acute myocardial infarction; Location of infarct
13.  Troponin-T levels and infarct size by SPECT myocardial perfusion imaging: a prospective evaluation 
JACC. Cardiovascular imaging  2011;4(5):523-533.
To evaluate the relationship between serial c-TnT levels with infarct size and left ventricular ejection fraction (LVEF) by gated single photon emission computed tomography myocardial perfusion imaging (SPECT-MPI) in patients with acute myocardial infarction (AMI).
Current guidelines recommend the use of troponin (c-Tn) as the biomarker of choice for diagnosis of AMI. Data relating c-TnT to SPECT-MPI in patients with AMI are limited.
A subset of patients with first AMI participating in a community-based cohort of AMI in Olmsted County, MN, were prospectively studied. Serial c-TnT levels were evaluated at presentation, <12 hours, 1 day, 2 days, and 3 days after onset of pain. Peak c-TnT was defined as the maximum c-TnT value.
121 patients (age 61 ± 13; 31% women) with AMI underwent gated SPECT-MPI at a median (25th percentile; 75th percentile) of 10 (5; 15) days post-AMI. The type of infarct was NSTEMI in 61% and 13 % were anterior in location. Median infarct size was 1% (0%; 11%) and median gated LVEF was 54% (47%; 60%). 59 patients (49% of the population) had no measurable infarction by SPECT-MPI. Independent predictors for measurable SPECT-MPI infarct size included c-TnT at days 1, 2, 3 and peak c-TnT, but not at presentation or < 12 hours. In ROC analysis the AUC was highest at day 3. ROC analysis demonstrated a cut-off of 1.5 ng/mL for peak c-TnT for detection of measurable infarct size.
In a community-based cohort of patients with first AMI, independent predictors of measurable SPECT-MPI infarct size included c-TnT at days 1, 2, 3 and peak c-TnT. In contrast, c-TnT at presentation and <12 hours were not independent predictors of MI size as assessed by SPECT-MPI. ROC analysis demonstrated a cut-off value peak c-TnT of 1.5 ng/mL for detection of measurable infarct.
PMCID: PMC3239221  PMID: 21565741
Imaging; myocardial infarction; scintigraphy; infarct size; troponin
14.  Hypokalemia-Induced Abnormal Movements: Case Report 
Trauma Monthly  2013;18(3):141-144.
A sudden loss of consciousness followed by abnormal movements can be ictal or syncopal in origin. Transient response by the brain to sudden decrease of blood flow may cause sudden loss of consciousness followed by abnormal movements that mimic seizure. Dysrhythmia is one of the important and critical reasons of such events that should be differentiated from seizure.
Case Presentation
In this case report we describe a 55 year-old woman admitted to our emergency department first with the impression of seizure. Eventually, it was realized that she had suffered from brain hypo-perfusion secondary to hypokalemia induced arrhythmia. Her arrhythmia was managed by unsynchronized biphasic shock in acute phase and also potassium replacement. She was then admitted to the CCU (Coronary Care Unit) where she received further care for medical management and drug dose adjustment and was discharged 4 days later.
Syncope from arrhythmia most commonly results from ventricular tachycardia, which accounts for 11% of all cases of syncope. Torsades de point is a unique type of ventricular tachycardia, characterized by QRS complexes of changing amplitude proceeded by prolonged QT intervals and almost often followed by loss of consciousness and also seizure like movements. Prolonged QT interval which is an important provocative factor for torsades de point commonly results from interactions between drug therapy, myocardial ischemia, and electrolyte disturbances such as hypokalemia or hypomagnesaemia. Changes in the extracellular potassium level have predominant and profound influences on the function of the cardiovascular system that may provoke fatal demonstrations such as QT prolongation, ventricular arrhythmia and even cardiac arrest. Electrolyte assessment is particularly important in certain patient populations, such as the elderly in whom a variety of pathological states or conditions like dehydration or renal failure are more common. Early identification and correction of these disturbances are necessary to control either seizures or seizure-like movements and prevent permanent brain damage, as anticonvulsants alone are generally ineffective.
PMCID: PMC3864401  PMID: 24350174
Hypokalemia; Arrhythmias, Cardiac; Seizures
15.  Risk of Death and Recurrent Ventricular Arrhythmias in Survivors of Cardiac Arrest Concurrent With Acute Myocardial Infarction 
Cardiac arrest (CA) is an indication for defibrillator (ICD) implantation unless it occurs in the context of an acute myocardial infarction (AMI). We investigated the ventricular arrhythmia (VA)-free survival of patients resuscitated from CA in the setting of AMI.
We reviewed a database of 1600 AMI and CA survivors from which 48 patients were identified as having concurrent CA and AMI (CA+AMI group). Those patients were matched by age, gender, race, and left ventricular ejection fraction (LVEF) to 96 patients with AMI but no CA (AMI group) and 48 patients with CA but no AMI (CA group).
Patients and controls were followed for 3.9±3.2 years. Patients in the 3 groups had similar baseline characteristics (age 63±14 yrs, 78% men, 98% white, 53% with CAD, LVEF 33±14%). The 5-year VA-free survival was 67%, 92%, and 80% for the CA+AMI, AMI, and CA groups, respectively, p<0.001.
Patients with concurrent CA and AMI are at high risk of recurrent VA, with VA-free survival rates significantly worse than those of patients with AMI but no CA, and comparable to those of patients with CA outside the context of an AMI. Accordingly, these patients should be considered for ICD implantation.
Condensed Abstract
Patients with concurrent CA and AMI were found to be at high risk of recurrent VA, with VA-free survival rates significantly worse than those of patients with AMI but no CA, and comparable to those with CA only. Accordingly, these patients should be considered for ICD implantation.
PMCID: PMC2231605  PMID: 18270598
Cardiac Arrest; Ventricular Arrhythmias; Myocardial Infarction; Defibrillators; Mortality
16.  Reduced levels of circulating endothelial progenitor cells in acute myocardial infarction patients with diabetes or pre-diabetes: accompanying the glycemic continuum 
Diabetic patients have a significantly worse prognosis after an acute myocardial infarction (AMI) than their counterparts. Previous studies have shown that the number of circulating endothelial progenitor cells (EPCs) significantly increase early after an AMI in normoglycemic patients. However, it is well known that type 2 diabetes mellitus (DM) is associated with impaired function and reduced circulating EPCs levels. Nonetheless, few studies have analyzed EPCs response of diabetics to an AMI and the EPC response of pre-diabetic patients has not been reported yet. Therefore, we hypothesized that in the acute phase of an AMI, diabetic and pre-diabetics have lower circulating EPCs levels than patients with normal glucose metabolism. We also evaluated the possible capacity of chronic antidiabetic treatment in the recovery of EPCs response to an AMI in diabetics.
One-hundred AMI patients were prospectively enrolled in the study. Using the high-performance flow cytometer FACSCanto II, circulating EPCs (CD45dimCD34+KDR+ and CD45dimCD133+KDR+ cells) were quantified, within the first 24 hours of admission. In addition, as an indirect functional parameter, we also analyzed the fraction of EPCs coexpressing the homing marker CXCR4.
We found that in the acute phase of an AMI, diabetic patients presented significantly lower levels of circulating CD45dimCD34+KDR+ and CD45dimCD133+KDR+ EPCs by comparison with nondiabetics, with a parallel decrease in the subpopulations CXCR4+ (p < 0.001). Indeed, this study suggests that the impaired response of EPCs to an AMI is an early event in the natural history of DM, being present even in pre-diabetes. Our results, also demonstrated that numbers of all EPCs populations were inversely correlated with HbA1c (r = -0.432, p < 0.001 for CD45dimCD34+KDR+ cells). Finally, this study suggests that previous chronic insulin therapy (but not oral antidiabetic drugs) attenuate the deficient response of diabetic EPCs to an AMI.
This study indicates that there is a progressive decrease in EPCs levels, from pre-diabetes to DM, in AMI patients. Moreover, glycemic control seems to be determinant for circulating EPCs levels presented in the acute phase of an AMI and chronic insulin therapy may probably attenuate the deficit in EPCs pool seen in diabetics.
PMCID: PMC4082424  PMID: 24934236
Endothelial progenitor cells; Diabetes; Pre-diabetes; Insulin; Oral antidiabetic drugs; Acute myocardial infarction; Homing
17.  Plasma Brain Natriuretic Peptide (BNP) as an Indicator of Left Ventricular Function, Early Outcome and Mechanical Complications after Acute Myocardial Infarction 
This study investigated the prognostic value of B type natriuretic peptide (BNP) in acute myocardial infarction (AMI) patients and its relation with left ventricular function and post-myocardial infarction complications.
In this cross-sectional study, plasma BNP level was measured for 42 consecutive patients (mean ± SD: 61.6 ± 10.85 years old) with acute ST elevation myocardial infarction (MI) and 42 healthy, age and gender matched subjects.
BNP level in AMI patients were significantly higher than control group (P < 0.001). Regarding to infarct location, the highest BNP level measured in inferoposterior MI (BNP = 4436.63 ± 6188.159 pg/ml) and the lowest one indicated in standalone inferior MI (BNP = 598.83 ± 309.867 pg/ml (P = 0.071). There was significant reverse relation between BNP and EF (P = 0.006, OR = −0.47) and a significant relationship between BNP and killip classification (P = 0.036). There was no significant relation between diastolic and right-ventricular function and BNP level (P = 0.61, P = 0.21). The highest BNP level was detected in LV septal rupture and false aneurysm (P = 0.02) and in ventricular tachycardia, but without significant relationship (P = 0.25).
After the onset of AMI, BNP blood level can be used as an important predictor for left ventricular dysfunction, killip classification, early mechanical complications and cardiac death.
PMCID: PMC3165920  PMID: 21912490
brain natriuretic peptide; acute myocardial infarction; mechanical heart complications; systolic dysfunction
18.  Advanced Electrophysiologic Mapping Systems 
Executive Summary
To assess the effectiveness, cost-effectiveness, and demand in Ontario for catheter ablation of complex arrhythmias guided by advanced nonfluoroscopy mapping systems. Particular attention was paid to ablation for atrial fibrillation (AF).
Clinical Need
Tachycardia refers to a diverse group of arrhythmias characterized by heart rates that are greater than 100 beats per minute. It results from abnormal firing of electrical impulses from heart tissues or abnormal electrical pathways in the heart because of scars. Tachycardia may be asymptomatic, or it may adversely affect quality of life owing to symptoms such as palpitations, headaches, shortness of breath, weakness, dizziness, and syncope. Atrial fibrillation, the most common sustained arrhythmia, affects about 99,000 people in Ontario. It is associated with higher morbidity and mortality because of increased risk of stroke, embolism, and congestive heart failure. In atrial fibrillation, most of the abnormal arrhythmogenic foci are located inside the pulmonary veins, although the atrium may also be responsible for triggering or perpetuating atrial fibrillation. Ventricular tachycardia, often found in patients with ischemic heart disease and a history of myocardial infarction, is often life-threatening; it accounts for about 50% of sudden deaths.
Treatment of Tachycardia
The first line of treatment for tachycardia is antiarrhythmic drugs; for atrial fibrillation, anticoagulation drugs are also used to prevent stroke. For patients refractory to or unable to tolerate antiarrhythmic drugs, ablation of the arrhythmogenic heart tissues is the only option. Surgical ablation such as the Cox-Maze procedure is more invasive. Catheter ablation, involving the delivery of energy (most commonly radiofrequency) via a percutaneous catheter system guided by X-ray fluoroscopy, has been used in place of surgical ablation for many patients. However, this conventional approach in catheter ablation has not been found to be effective for the treatment of complex arrhythmias such as chronic atrial fibrillation or ventricular tachycardia. Advanced nonfluoroscopic mapping systems have been developed for guiding the ablation of these complex arrhythmias.
The Technology
Four nonfluoroscopic advanced mapping systems have been licensed by Health Canada:
CARTO EP mapping System (manufactured by Biosense Webster, CA) uses weak magnetic fields and a special mapping/ablation catheter with a magnetic sensor to locate the catheter and reconstruct a 3-dimensional geometry of the heart superimposed with colour-coded electric potential maps to guide ablation.
EnSite System (manufactured by Endocardial Solutions Inc., MN) includes a multi-electrode non-contact catheter that conducts simultaneous mapping. A processing unit uses the electrical data to computes more than 3,000 isopotential electrograms that are displayed on a reconstructed 3-dimensional geometry of the heart chamber. The navigational system, EnSite NavX, can be used separately with most mapping catheters.
The LocaLisa Intracardiac System (manufactured by Medtronics Inc, MN) is a navigational system that uses an electrical field to locate the mapping catheter. It reconstructs the location of the electrodes on the mapping catheter in 3-dimensional virtual space, thereby enabling an ablation catheter to be directed to the electrode that identifies abnormal electric potential.
Polar Constellation Advanced Mapping Catheter System (manufactured by Boston Scientific, MA) is a multielectrode basket catheter with 64 electrodes on 8 splines. Once deployed, each electrode is automatically traced. The information enables a 3-dimensional model of the basket catheter to be computed. Colour-coded activation maps are reconstructed online and displayed on a monitor. By using this catheter, a precise electrical map of the atrium can be obtained in several heartbeats.
Review Strategy
A systematic search of Cochrane, MEDLINE and EMBASE was conducted to identify studies that compared ablation guided by any of the advanced systems to fluoroscopy-guided ablation of tachycardia. English-language studies with sample sizes greater than or equal to 20 that were published between 2000 and 2005 were included. Observational studies on safety of advanced mapping systems and fluoroscopy were also included. Outcomes of interest were acute success, defined as termination of arrhythmia immediately following ablation; long-term success, defined as being arrhythmia free at follow-up; total procedure time; fluoroscopy time; radiation dose; number of radiofrequency pulses; complications; cost; and the cost-effectiveness ratio.
Quality of the individual studies was assessed using established criteria. Quality of the overall evidence was determined by applying the GRADE evaluation system. (3) Qualitative synthesis of the data was performed. Quantitative analysis using Revman 4.2 was performed when appropriate.
Quality of the Studies
Thirty-four studies met the inclusion criteria. These comprised 18 studies on CARTO (4 randomized controlled trials [RCTs] and 14 non-RCTs), 3 RCTs on EnSite NavX, 4 studies on LocaLisa Navigational System (1 RCT and 3 non-RCTs), 2 studies on EnSite and CARTO, 1 on Polar Constellation basket catheter, and 7 studies on radiation safety.
The quality of the studies ranged from moderate to low. Most of the studies had small sample sizes with selection bias, and there was no blinding of patients or care providers in any of the studies. Duration of follow-up ranged from 6 weeks to 29 months, with most having at least 6 months of follow-up. There was heterogeneity with respect to the approach to ablation, definition of success, and drug management before and after the ablation procedure.
Summary of Findings
Evidence is based on a small number of small RCTS and non-RCTS with methodological flaws.
Advanced nonfluoroscopy mapping/navigation systems provided real time 3-dimensional images with integration of anatomic and electrical potential information that enable better visualization of areas of interest for ablation
Advanced nonfluoroscopy mapping/navigation systems appear to be safe; they consistently shortened the fluoroscopy duration and radiation exposure.
Evidence suggests that nonfluoroscopy mapping and navigation systems may be used as adjuncts to rather than replacements for fluoroscopy in guiding the ablation of complex arrhythmias.
Most studies showed a nonsignificant trend toward lower overall failure rate for advanced mapping-guided ablation compared with fluoroscopy-guided mapping.
Pooled analyses of small RCTs and non-RCTs that compared fluoroscopy- with nonfluoroscopy-guided ablation of atrial fibrillation and atrial flutter showed that advanced nonfluoroscopy mapping and navigational systems:
Yielded acute success rates of 69% to 100%, not significantly different from fluoroscopy ablation.
Had overall failure rates at 3 months to 19 months of 1% to 40% (median 25%).
Resulted in a 10% relative reduction in overall failure rate for advanced mapping guided-ablation compared to fluoroscopy guided ablation for the treatment of atrial fibrillation.
Yielded added benefit over fluoroscopy in guiding the ablation of complex arrhythmia. The advanced systems were shown to reduce the arrhythmia burden and the need for antiarrhythmic drugs in patients with complex arrhythmia who had failed fluoroscopy-guided ablation
Based on predominantly observational studies, circumferential PV ablation guided by a nonfluoroscopy system was shown to do the following:
Result in freedom from atrial fibrillation (with or without antiarrhythmic drug) in 75% to 95% of patients (median 79%). This effect was maintained up to 28 months.
Result in freedom from atrial fibrillation without antiarrhythmic drugs in 47% to 95% of patients (median 63%).
Improve patient survival at 28 months after the procedure as compared with drug therapy.
Require special skills; patient outcomes are operator dependent, and there is a significant learning curve effect.
Complication rates of pulmonary vein ablation guided by an advanced mapping/navigation system ranged from 0% to 10% with a median of 6% during a follow-up period of 6 months to 29 months.
The complication rate of the study with the longest follow-up was 8%.
The most common complications of advanced catheter-guided ablation were stroke, transient ischemic attack, cardiac tamponade, myocardial infarction, atrial flutter, congestive heart failure, and pulmonary vein stenosis. A small number of cases with fatal atrial-esophageal fistula had been reported and were attributed to the high radiofrequency energy used rather than to the advanced mapping systems.
Economic Analysis
An Ontario-based economic analysis suggests that the cumulative incremental upfront costs of catheter ablation of atrial fibrillation guided by advanced nonfluoroscopy mapping could be recouped in 4.7 years through cost avoidance arising from less need for antiarrhythmic drugs and fewer hospitalization for stroke and heart failure.
Expert Opinion
Expert consultants to the Medical Advisory Secretariat noted the following:
Nonfluoroscopy mapping is not necessary for simple ablation procedures (e.g., typical flutter). However, it is essential in the ablation of complex arrhythmias including these:
Symptomatic, drug-refractory atrial fibrillation
Arrhythmias in people who have had surgery for congenital heart disease (e.g., macro re-entrant tachycardia in people who have had surgery for congenital heart disease).
Ventricular tachycardia due to myocardial infarction
Atypical atrial flutter
Advanced mapping systems represent an enabling technology in the ablation of complex arrhythmias. The ablation of these complex cases would not have been feasible or advisable with fluoroscopy-guided ablation and, therefore, comparative studies would not be feasible or ethical in such cases.
Many of the studies included patients with relatively simple arrhythmias (e.g., typical atrial flutter and atrial ventricular nodal re-entrant tachycardia), for which the success rates using the fluoroscopy approach were extremely high and unlikely to be improved upon using nonfluoroscopic mapping.
By age 50, almost 100% of people who have had surgery for congenital heart disease will develop arrhythmia.
Some centres are under greater pressure because of expertise in complex ablation procedures for subsets of patients.
The use of advanced mapping systems requires the support of additional electrophysiologic laboratory time and nursing time.
For patients suffering from symptomatic, drug-refractory atrial fibrillation and are otherwise healthy, catheter ablation offers a treatment option that is less invasive than is open surgical ablation.
Small RCTs that may have been limited by type 2 errors showed significant reductions in fluoroscopy exposure in nonfluoroscopy-guided ablation and a trend toward lower overall failure rate that did not reach statistical significance.
Pooled analysis suggests that advanced mapping systems may reduce the overall failure rate in the ablation of atrial fibrillation.
Observational studies suggest that ablation guided by complex mapping/navigation systems is a promising treatment for complex arrhythmias such as highly symptomatic, drug-refractory atrial fibrillation for which rate control is not an option
In people with atrial fibrillation, ablation guided by advanced nonfluoroscopy mapping resulted in arrhythmia free rates of 80% or higher, reduced mortality, and better quality of life at experienced centres.
Although generally safe, serious complications such as stroke, atrial-esophageal, and pulmonary vein stenosis had been reported following ablation procedures.
Experts advised that advanced mapping systems are also required for catheter ablation of:
Hemodynamically unstable ventricular tachycardia from ischemic heart disease
Macro re-entrant atrial tachycardia after surgical correction of congenital heart disease
Atypical atrial flutter
Catheter ablation of atrial fibrillation is still evolving, and it appears that different ablative techniques may be appropriate depending on the characteristics of the patient and the atrial fibrillation.
Data from centres that perform electrophysiological mapping suggest that patients with drug-refractory atrial fibrillation may be the largest group with unmet need for advanced mapping-guided catheter ablation in Ontario.
Nonfluoroscopy mapping-guided pulmonary vein ablation for the treatment of atrial fibrillation has a significant learning effect; therefore, it is advisable for the province to establish centres of excellence to ensure a critical volume, to gain efficiency and to minimize the need for antiarrhythmic drugs after ablation and the need for future repeat ablation procedures.
PMCID: PMC3379531  PMID: 23074499
19.  Ischemic Ventricular Arrhythmias Experimental Models and Their Clinical Relevance 
In the United States, sudden cardiac death accounts for an estimated 300,000 to 350,000 cases each year, 80,000 presenting as the first manifestation of a preexisting, sometimes unrecognized, coronary artery disease. Acute-myocardial infarction (AMI)-induced ventricular fibrillation (VF) frequently occurs without warning, often leading to death within minutes in patients who do not receive prompt medical attention.
Identification of patients at risk of AMI-induced lethal ventricular arrhythmias remains an unmet medical need. Recent studies suggest that a genetic predisposition may significantly contribute to the vulnerability of the ischemic myocardium to ventricular tachycardia (VT)/VF.
Numerous experimental models have been developed for the purpose of advancing our understanding of the mechanisms responsible for the development of cardiac arrhythmias in the setting of ischemia and with the aim of identifying antiarrhythmic therapies that could be of clinically benefit. While our understanding of the mechanisms underlying AMI-induced ventricular arrhythmias is coming into better focus, risk stratification of patients with AMI remains a major challenge.
This review briefly discusses our current state of knowledge regarding the mechanisms of ischemic ventricular arrhythmias and their temporal distribution as revealed by available experimental models, how these correlate with the clinical syndromes, as well as prospective prophylactic therapies for the prevention and treatment of ischemia-induced life-threatening arrhythmias.
PMCID: PMC3222739  PMID: 21740880
Acute Myocardial Infarction; Ischemia; Ventricular Fibrillation; Sudden Cardiac Death; Electrophysiology
20.  Prediction of fatal or near-fatal cardiac arrhythmia events in patients with depressed left ventricular function after an acute myocardial infarction† 
European Heart Journal  2009;30(6):689-698.
To determine whether risk stratification tests can predict serious arrhythmic events after acute myocardial infarction (AMI) in patients with reduced left ventricular ejection fraction (LVEF ≤ 0.40).
Methods and results
A total of 5869 consecutive patients were screened in 10 European centres, and 312 patients (age 65 ± 11 years) with a mean LVEF of 31 ± 6% were included in the study. Heart rate variability/turbulence, ambient arrhythmias, signal-averaged electrocardiogram (SAECG), T-wave alternans, and programmed electrical stimulation (PES) were performed 6 weeks after AMI. The primary endpoint was ECG-documented ventricular fibrillation or symptomatic sustained ventricular tachycardia (VT). To document these arrhythmic events, the patients received an implantable ECG loop-recorder. There were 25 primary endpoints (8.0%) during the follow-up of 2 years. The strongest predictors of primary endpoint were measures of heart rate variability, e.g. hazard ratio (HR) for reduced very-low frequency component (<5.7 ln ms2) adjusted for clinical variables was 7.0 (95% CI: 2.4–20.3, P < 0.001). Induction of sustained monomorphic VT during PES (adjusted HR = 4.8, 95% CI, 1.7–13.4, P = 0.003) also predicted the primary endpoint.
Fatal or near-fatal arrhythmias can be predicted by many risk stratification methods, especially by heart rate variability, in patients with reduced LVEF after AMI.
PMCID: PMC2655314  PMID: 19155249
Sudden cardiac death; Heart rate; Variability; Implantable cardioverter-defibrillator
21.  Clinical Significance of Conditions Presenting with ECG Changes Mimicking Acute Myocardial Infarction 
The electrocardiogram (ECG) is the primary tool in the diagnosis of acute myocardial infarction (AMI). However, other clinical conditions, both cardiac and noncardiac originated pathologies, may result in ECG tracing of AMI. This may lead to an incorrect diagnosis, exposing the patients to unnecessary tests and potentially harmful therapeutic procedures. The aim of this report is to increase the still insufficient awareness of clinicians from multiple disciplines, regarding the different clinical syndromes, both cardiac and noncardiac, associated with ECG abnormalities mimicking AMI, to avoid unjustified thrombolytic therapy or intervention procedures. During a 9-year period, the data from six patients (five females, one male; mean age, 50 years [range, 18 to 78 years]) who were admitted to cardiac care unit (CCU) with transient ECG changes resembling AMI were recorded retrospectively. During this 9-year period, 5,400 patients were hospitalized in CCU: 1,350 patients were diagnosed as ST-elevation myocardial infarction (STEMI) and 4,050 patients were diagnosed as non-ST-elevation myocardial infarction (NSTEMI). Only two out of six patients had chest pain with ECG changes criteria suspicious of AMI. STEMI was suspected in four out of six patients. All patients, but one, had normal left ventricular (LV) function. One patient had transient LV dysfunction. All patients, but one, with perimyocarditis, had normal serum cardiac markers. In four out of six patients, who underwent coronary arteries imaging during hospitalization (by angiography or by CT scan), normal coronary arteries were documented. Two patients who underwent ambulatory cardiac CT scan imaging after being discharged from hospital documented patent coronary arteries (case no. 3), or some insignificant irregularities (case no. 4). The discharge diagnoses from CCU were as follows: postictal syndrome, pericarditis, hypothermia, stress-induced (“tako-tsubo”) cardiomyopathy, anaphylactic reaction, and status of postchemotherapy. All patients experienced full recovery with normal ECG tracing. During the 5-year follow-up, all patients were alive, and cardiac morbidity was not reported. We conclude that both cardiac and noncardiac clinical syndromes may mimic AMI. Comprehensive clinical examination and profound medical history are crucial for making the correct diagnosis in conditions with ECG changes mimicking AMI.
PMCID: PMC3709959  PMID: 24436595
ECG changes; mimicking acute MI; clinical conditions; cardiac and noncardiac; normal coronary arteries
22.  Polymorphic ventricular tachycardia in acute myocardial infarction treated by thrombolysis: reperfusion, complication or iatrogenic sign? 
Mædica  2010;5(2):142-145.
The QT interval prolongation may determine a type of polymorphic ventricular tachycardia named torsades de pointes. This ventricular arrhythmia could also appear after thrombolysis of acute myocardial infarction.
Case reports. A 57 years old man was admitted 2 hours after the onset of a posterior-inferior-lateral acute myocardial infarction (reinfarction). He underwent pharmacological revascularization with reteplase. In the first 24 hours after thrombolysis a sustained polymorphic ventricular tachycardia was unregistered after the second dose of a quinolone recommended for a urological problem. Despite of the normal serum potassium and magnesium QTc suffered an augmentation from 400 ms to 480 ms. After beta-blocker augmentation dose and the antibiotic changing, ventricular arrhythmia disappeared without repetition during hospitalization. This ventricular tachycardia was considered precipitated by the quinolones therapy by increasing of QTc interval. It could also be considered a reperfusion sign or a complication of the reinfarction in the same area, which means different therapeutical solutions.
PMCID: PMC3150014  PMID: 21977140
polymorphic ventricular tachycardia; quinolones; thrombolysis; acute myocardial infarction
23.  Left Ventricular Systolic and Diastolic Function in Patients With Apical Ballooning Syndrome Compared With Patients With Acute Anterior ST-Segment Elevation Myocardial Infarction: A Functional Paradox 
Mayo Clinic Proceedings  2009;84(6):514-521.
OBJECTIVE: To compare left ventricular (LV) systolic and diastolic function in patients with apical ballooning syndrome (ABS) and those with acute myocardial infarction (AMI) using 2-dimensional Doppler echocardiography and strain rate imaging (SRI).
PATIENTS AND METHODS: We prospectively enrolled patients with newly diagnosed AMI and ABS who had akinetic apical walls. Both 2-dimensional Doppler echocardiography and SRI were performed on hospital day 1 or within 24 hours of primary percutaneous coronary intervention.
RESULTS: Twenty-four patients with AMI and 13 patients with ABS (mean ± SD age, 63±15 vs 73±12 years; P=.03) were prospectively enrolled in the study from October 3, 2005 through July 12, 2006. The mean ± SD LV end-diastolic volume was larger (58.1±9.1 vs 45.2±10.6 mL/m2; P<.001) and the mean ± SD LV ejection fraction was lower (35%±6% vs 43%±9%; P=.006) in patients with ABS compared with patients with AMI. The early diastolic mitral annular velocity was similar (0.06±0.02 vs 0.06±0.02 m/s; P=.85) in both groups, but the ratio of early diastolic mitral valve inflow velocity to early diastolic mitral annulus velocity was higher in patients with AMI than in patients with ABS (16.3±6.9 vs 12.2±3.2; P=.05). The systolic strain rate was decreased at the apex in both groups (P=.98). Both the early diastolic strain rate of the apex (0.64±0.24 vs 0.48±0.30 s-1; P=.04) and the postsystolic shortening index of the apex (61%±15% vs 45%±23%; P=.006) were higher in the patients with ABS than in those with AMI. However, early diastolic SR was higher in the akinetic apical walls of patients with AMI with recovery than those with no recovery (0.64±0.35 vs 0.43±0.25 s-1; P=.04) and was similar between akinetic apical walls of patients with AMI with recovery and the akinetic apical walls of ABS.
CONCLUSION: Compared with patients with AMI, those with ABS showed the functional paradox of worse initial LV systolic function with larger LV size but better LV diastolic function. The early systolic strain rate and postsystolic shortening were greater in patients with ABS than in those with AMI; hence, these measurements can be helpful in distinguishing ABS from AMI and in detecting myocardial viability.
Compared with patients with acute myocardial infarction, those with apical ballooning syndrome showed the functional paradox of worse initial left ventricular (LV) systolic function with larger LV size but better LV diastolic function. The early systolic strain rate and postsystolic shortening were greater in patients with apical ballooning syndrome than in those with acute myocardial infarction.
PMCID: PMC2688625  PMID: 19483168
24.  Association of ventricular extrasystoles and ventricular tachycardia with idioventricular rhythm. 
British Heart Journal  1976;38(5):457-464.
Patients with acute myocardial infarction were monitored for ventricular arrhythmias in the first 48 hours. Idioventricular rhythm (rate less than 100/minute) occurred in 35 out of 224 patients (15.6%) during the first day and in 13 out of 192 patients not receiving treatment on the second day (6.8%). This arrhythmia was frequently preceded by late ventricular extrasystoles, which often showed variation of their coupling intervals to the preceding QRS. Double ventricular extrasystoles separated by larger than or equal to 600 ms were also precursors of idioventricular rhythm. Idioventricular rhythm at times could be described as an escape rhythm, but on other occasions it was undoubtedly an accelerated rhythm. Spontaneous changes in the idioventricular cycle length were frequent on single one-minute electrocardiographic recordings. The rate of the dominant rhythm in patients with episodes of idioventricular rhythm was significantly slower than the heart rate of patients without this arrhythmia. Idioventricular rhythm was more frequent in patients with inferior infarction. Idioventricular rhythm sometimes preceded ventricular tachycardia but there was only a significant association between ventricular tachycardia and idioventricular rhythms with rates of over 75/minute. Irregular idioventricular rhythm frequently accelerated to ventricular tachycardia. It is suggested that the term benign idioventricular rhythm be reserved for those rhythms below 75/minute, and that the term rapid idioventricular rhythm should be used for rhythms between 75 and 120/minute. The rate of idioventricular rhythm is related to the probability of development of life-threatening ventricular arrhythmias during the first 48 hours after myocardial infarction.
PMCID: PMC483017  PMID: 57785
25.  Plasma exchange successfully treats central pontine myelinolysis after acute hypernatremia from intravenous sodium bicarbonate therapy 
BMC Nephrology  2014;15:56.
Osmotic demyelination syndrome (ODS) primarily occurs after rapid correction of severe hyponatremia. There are no proven effective therapies for ODS, but we describe the first case showing the successful treatment of central pontine myelinolysis (CPM) by plasma exchange, which occurred after rapid development of hypernatremia from intravenous sodium bicarbonate therapy.
Case presentation
A 40-year-old woman presented with general weakness, hypokalemia, and metabolic acidosis. The patient was treated with oral and intravenous potassium chloride, along with intravenous sodium bicarbonate. Although her bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed hypernatremia with serum sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing hypernatremia, she exhibited tetraparesis, drooling, difficulty swallowing, and dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of hypernatremia after intravenous sodium bicarbonate therapy and treated her with plasma exchange. After two consecutive plasma exchange sessions, her neurologic symptoms were markedly improved except for mild diplopia. After the plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap metabolic acidosis, low blood bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a sodium bicarbonate loading test and diagnosed distal renal tubular acidosis (RTA). We also found that she had Sjögren’s syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer’s test and a lower lip biopsy. She was discharged and treated as an outpatient with oral sodium bicarbonate and potassium chloride.
This case indicates that serum sodium concentrations should be carefully monitored in patients with distal RTA receiving intravenous sodium bicarbonate therapy. We should keep in mind that acute hypernatremia and CPM can be associated with intravenous sodium bicarbonate therapy, and that CPM due to acute hypernatremia may be effectively treated with plasma exchange.
PMCID: PMC3986463  PMID: 24708786
Central pontine myelinolysis; Hypernatremia; Plasma exchange; Renal tubular acidosis; Sjögren’s syndrome; Sodium bicarbonate

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