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.
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.
Inferior Acute Myocardial Infarction; Left Ventricular Ejection Fraction; Streptokinase; Mortality Rate
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.
polymorphic ventricular tachycardia; quinolones; thrombolysis; acute myocardial infarction
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.
Sudden cardiac death; Heart rate; Variability; Implantable cardioverter-defibrillator
Cardiovascular diseases are the major causes of mortality worldwide and acute myocardial infarction (AMI) is the leading cause of mortality among cardiovascular diseases. Thrombolytic therapies, especially during the first few hours after the disease onset, can significantly reduce AMI-related mortality.
The current study aimed to determine the prevalence and causes of non-administration of thrombolytic therapy for AMI patients admitted to Hajar Hospital, Shahrekord, Iran, from May until November 2000. Non-probability convenient sampling method was used to select 106 subjects with Q-wave AMI. Data was collected by completing a questionnaire, reviewing medical records, and interviewing with patients. SPSS7.5 was for data analysis.
A total number of 106 AMI patients were studied among whom 62 (59%) individuals received thrombolytic therapy. Delayed referral to the hospital was the major cause of failure to provide thrombolytic therapy. The cause of non-treatment could not be identified in 15 (19.5%) subjects eligible to receive therapy.
Training general practitioners and individuals involved in this regard along with accelerating the process of patient referral to hospitals can reduce AMI-related mortality.
Acute Myocardial Infarction; Thrombolytic; Therapy
At the Istituto di Clinica Medica Generale e Cardiologia (Florence, Italy), the widespread use of percutaneous coronary intervention (PCI) has markedly changed the hospital course of patients with acute myocardial infarction (AMI). These patients are typically transferred to the coronary care unit (CCU) only after primary PCI, whereas during the thrombolytic era, patients were first admitted to CCU before reperfusion.
OBJECTIVES AND METHODS
The incidence, timing and setting of complications from symptom onset to hospital discharge in 689 consecutive AMI patients undergoing PCI were evaluated.
Ventricular fibrillation occurred in 11% of patients, and most episodes (94.7%) occurred before or during PCI. Of all patients, 6.3% developed complete atrioventricular block (CAVB), and in 86.3% of these cases, the CAVB occurred before or during PCI; in 94.5%, a CAVB resolution occurred in the catheterization laboratory (CL). Thirty-one patients (4.5%) had impending shock on admission to the CL. Cardiogenic shock developed in 29 patients (4.2%), mostly in the prehospital phase or in the CL. Only four patients (less than 1%) developed cardiogenic shock later during their hospital course. Similarly, circulatory and ventilatory support, as well as temporary pacing and cardiac defibrillation, were used mostly in the prehospital phase or in the CL. During the CCU stay, 45 patients (6.5%) had hemorrhagic or vascular complications, and the incidence of post-PCI ischemia and early reocclusion of the culprit vessel were low (2.1% and 0.6%, respectively). Thus, cardiac complications usually associated with AMI were observed mainly before hospital admission or in the CL during the reopening of the target vessel. These complications were rarely observed after a successful PCI.
For AMI patients, the CL is not only the site of PCI, it is also where most life-threatening cardiac complications are observed and treated.
Angioplasty; Complications; Myocardial infarction
Acute myocardial infarction (AMI) is common in patients with diabetes. Reasons for this are multifactorial, but all relate to a variety of maladaptive responses to acute hyperglycemia. Persistent hyperglycemia is associated with worse left ventricular function and higher mortality during AMI, but intervention data are far from clear. Although there is a theoretical basis for the use of glucose-insulin-potassium infusion during AMI, lack of outcome efficacy (and inability to reach glycemic targets) in recent randomized trials has resulted in little enthusiasm for this strategy. Based on the increasing understanding of the dangers of hypoglycemia, while at the same time appreciating the role of hyperglycemia in AMI patients, goal glucose levels of 140–180 mg/dL using an intravenous insulin infusion while not eating seem reasonable for most patients and hospital systems. Non-glycemic therapy for patients with diabetes and AMI has benefited from more conclusive data, as this population has greater morbidity and mortality than those without diabetes. For ST-elevation myocardial infarction (STEMI), reperfusion therapy with primary percutaneous coronary intervention or fibrinolysis, antithrombotic therapy to prevent acute stent thrombosis following percutaneous coronary intervention or rethrombosis following thrombolysis, and initiation of β-blocker therapy are the current standard of care. Emergency coronary artery bypass graft surgery is reserved for the most critically ill. For those with non-STEMI, initial reperfusion therapy or fibrinolysis is not routinely indicated. Overall, there have been dramatic advances for the treatment of people with AMI and diabetes. The use of continuous glucose monitoring in this population may allow better ability to safely reach glycemic targets, which it is hoped will improve glycemic control.
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.
Ventricular tachycardia; fibrillation; arrhythmia; ischemia; sudden cardiac death
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.
Acute myocardial infarction (AMI) is currently one of the most important health problems in many countries around the world. Following AMI, many cytokines and proteolytic enzymes are released. Among these, matrix metalloproteinases (MMPs) are important proteolytic enzymes that lead to degradation of the extracellular matrix and to changes in cardiomyocytes in both infarcted and noninfarcted myocardium. This process is known as cardiac remodelling. It has been demonstrated that more than one type of MMP is present in the circulation after cardiomyocyte injury. A number of studies have demonstrated the correlations between these MMP levels and the severity of a coronary lesion, the progression of left ventricular dimension and the survival rate following AMI in both animal and human studies. MMPs have also been proposed as a possible novel prognostic indicator for myocardial infarction patients. Although the use of MMP inhibitors to improve cardiac outcome in AMI patients has been investigated, discrepancies in the results from those studies indicate that further research is still needed to warrant their beneficial effects. In the present review article, the roles of MMPs as prognostic indicators, as well as the factors influencing MMP expression, are discussed. Current findings on the role of MMP inhibitors in cardiac remodelling and the prognosis after AMI in both animal models and clinical studies are also examined.
Metalloproteinases; Myocardial infarction; Remodelling
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.
Acute Myocardial Infarction; Ischemia; Ventricular Fibrillation; Sudden Cardiac Death; Electrophysiology
Direct admission to Coronary Care Unit (CCU) on hospital arrival can be considered as a good proxy for adequate management in patients with acute myocardial infarction (AMI), as it has been associated with better prognosis. We analyzed a cohort of patients with AMI hospitalized in Rome (Italy) in 1997–2000 to assess the proportion directly admitted to CCU and to investigate the effect of patient characteristics such as gender, age, illness severity on admission, and socio-economic status (SES) on CCU admission practices.
Using discharge data, we analyzed a cohort of 9127 AMI patients. Illness severity on admission was determined using the Deyo's adaptation of the Charlson's comorbidity index, and each patient was assigned to one to four SES groups (level I referring to the highest SES) defined by a socioeconomic index, derived by the characteristics of the census tract of residence. The effect of gender, age, illness severity and SES, on risk of non-admission to CCU was investigated using a logistic regression model (OR, CI 95%).
Only 53.9% of patients were directly admitted to CCU, and access to optimal care was more frequently offered to younger patients (OR = 0.35; 95%CI = 0.25–0.48 when comparing 85+ to >=50 years), those with less severe illness (OR = 0.48; 95%CI = 0.37–0.61 when comparing Charlson index 3+ to 0) and the socially advantaged (OR = 0.81; 95%CI = 0.66–0.99 when comparing low to high SES).
In Rome, Italy, standard optimal coronary care is underprovided. It seems to be granted preferentially to the better off, even after controversial clinical criteria, such as age and severity of illness, are taken into account.
Left ventricular ejection fraction (LVEF) has been considered a major determinant of early outcome in acute myocardial infarction (AMI). Myocardial performance index (MPI) has been associated to early evolution in AMI in a heterogeneous population, including non ST-elevation or previous AMI. Left atrial volume has been related with late evolution after AMI. We evaluated the independent role of clinical and echocardiographic variables including LVEF, MPI and left atrial volume in predicting early in-hospital congestive heart failure (CHF) specifically in patients with a first isolated ST-elevation AMI.
Echocardiography was performed within 30 hours of chest pain in 95 patients with a first ST-elevation AMI followed during the first week of hospitalization. Several clinical and echocardiographic variables were analyzed. CHF was defined as Killip class ≥ II. Multivariate regression analysis was used to select independent predictor of in-hospital CHF.
Early in-hospital CHF occurred in 29 (31%) of patients. LVEF ≤ 0.45 was the single independent and highly significant predictor of early CHF among other clinical and echocardiographic variables (odds ratio 17.0; [95% CI 4.1 - 70.8]; p < 0.0001). MPI alone could not predict CHF in first ST-elevation AMI patients. Left atrial volume was not associated with early CHF in such patients.
For patients with first, isolated ST-elevation AMI, LVEF assessed by echocardiography still constitutes a strong and accurate independent predictor of early in-hospital CHF, superior to isolated MPI and left atrial volume in this particular subset of patients.
acute myocardial infarction; echocardiography; myocardial performance index; left atrial volume; ejection fraction
The aim of the present study was to compare circulating levels of selected prothrombotic markers in patients suffering acute myocardial infarction (AMI) with and without left ventricular (LV) thrombus.
One hundred patients with AMI treated with PCI on the LAD and dual antiplatelet therapy were included. LV thrombus formation was detected by echocardiography and/or MRI in 15 patients. Fasting blood samples were drawn 4–5 days (baseline), 6–7 days, 8–9 days, 2–3 weeks and 3 months after the AMI for determination of haemostatic markers.
We found higher levels of soluble tissue factor (TF) and D-dimer in the LV thrombus group 4–5 days, 8–9 days and 3 months (only TF) after the AMI compared to the patients without thrombus formation (p<0.05). Patients with TF in the upper quartile at baseline had significantly higher risk for LV thrombus (OR 4.2; 95% CI 1.2 -14.5; p=0.02, adjusted for infarct size).
The levels of prothrombin fragment 1+2 (F1+2) and endogenous thrombin potential (ETP) were significantly lower in the thrombus group after 8–9 days (only ETP), 2–3 weeks and 3 months. The levels of plasminogen activator inhibitor 1 activity and tissue plasminogen activator antigen did not differ between the groups.
In the acute phase of AMI, we found higher levels of TF and D-dimer in the LV thrombus group, indicating hypercoagulability of possible importance for the generation of mural thrombus. Lower levels of F1+2, ETP and D-dimer in the thrombus group late during follow-up are probably induced by the initiated anticoagulation therapy.
Acute myocardial infarction; Haemostatic markers; Inflammation; Left ventricular thrombus formation
Congestive heart failure developing after acute myocardial infarction (AMI) is a major cause of morbidity and mortality. Clinical trials of cell-based therapy after AMI evidenced only a moderate benefit. We could show previously that suspensions of apoptotic peripheral blood mononuclear cells (PBMC) are able to reduce myocardial damage in a rat model of AMI. Here we experimentally examined the biochemical mechanisms involved in preventing ventricular remodelling and preserving cardiac function after AMI. Cell suspensions of apoptotic cells were injected intravenously or intramyocardially after experimental AMI induced by coronary artery ligation in rats. Administration of cell culture medium or viable PBMC served as controls. Immunohistological analysis was performed to analyse the cellular infiltrate in the ischaemic myocardium. Cardiac function was quantified by echocardiography. Planimetry of the infarcted hearts showed a significant reduction of infarction size and an improvement of post AMI remodelling in rats treated with suspensions of apoptotic PBMC (injected either intravenously or intramoycardially). Moreover, these hearts evidenced enhanced homing of macrophages and cells staining positive for c-kit, FLK-1, IGF-I and FGF-2 as compared to controls. A major finding in this study further was that the ratio of elastic and collagenous fibres within the scar tissue was altered in a favourable fashion in rats injected with apoptotic cells. Intravenous or intramyocardial injection of apoptotic cell suspensions results in attenuation of myocardial remodelling after experimental AMI, preserves left ventricular function, increases homing of regenerative cells and alters the composition of cardiac scar tissue. The higher expression of elastic fibres provides passive energy to the cardiac scar tissue and results in prevention of ventricular remodelling.
Electronic supplementary material
The online version of this article (doi:10.1007/s00395-011-0173-0) contains supplementary material, which is available to authorized users.
Myocardial infarction; Apoptosis; Cytokines; Cell therapy; Elastin; Collagen
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.
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.
amantadine; overdose; torsades; hypokalemia
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.
Imaging; myocardial infarction; scintigraphy; infarct size; troponin
To determine if an early regular cardiac rehabilitation program would have an adverse effect on myocardial function after acute myocardial infarction (AMI).
Patients who received percutaneous coronary intervention (PCI) after AMI were divided into the exercise group and control group in accordance with their willingness to participate. Patients in the exercise group (n=18) received ECG monitored exercise for six weeks and were instructed to maintain self exercise in their communities for four months. The control group (n=16) patients were just instructed of risk factor control. All the subjects underwent echocardiography at the time of the AMI as well as six months later. The echocardiography parameters, including the left ventricular ejection fraction (LVEF), stroke volume (SV), left ventricular end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD), were measured.
In the exercise group, the LVEF increased to 59.58±9.24% and 61.58±9.63% after six weeks and six months, respectively (p<0.05), but SV, LVEDD and LVESD did not change (p>0.05).
Active participation in the cardiac rehabilitation program approximately two weeks after AMI did not have an adverse effect on the size of the left ventricle and myocardial function.
Myocardial infarction; Rehabilitation; Exercise; Left ventricular remodeling
Although medical comorbidities commonly affect clinical outcomes after acute myocardial infarction (AMI), current performance measures of AMI quality focus exclusively on management of the AMI itself. However, AMI patients frequently present with other comorbidities such as diabetes mellitus (DM) that also warrant assessment and management. To date, the quality of DM evaluation among patients presenting with an AMI has not been described. Between 1/2003-6/2004, the PREMIER-QI registry enrolled 3953 AMI patients at 19 U.S. centers. Frequency of glycosylated hemoglobin (A1C) assessment, either during the hospitalization or documented in the chart from the preceding 3 months, was prospectively evaluated. Among 1168 AMI patients with pre-existing DM, only 47% had recent A1C levels available, with marked variability in A1C assessment between hospitals (range 7%–81%). Among those with available A1C, 39% had good control (A1C <7), 36% suboptimal control (A1C 7–9), and 25% poor control (A1C >9). Patients with suboptimal and poor control were more likely to have their DM treatment intensified than those without A1C assessment (RR 1.38 [CI 1.03–1.85] for A1C 7–9; RR 2.20 [CI 1.68–2.88] for A1C >9). Similarly, patients with DM who had A1C measured were more likely to receive instructions on DM disease management prior to discharge. In conclusion, assessment of chronic glycemic control is highly variable among AMI patients with DM. Since much of this variability occurs at the hospital level, evaluation of DM control could represent an additional quality indicator and an opportunity to advance patient-centered AMI care.
Myocardial infarction; diabetes mellitus; glycosylated hemoglobin
Acute myocardial ischemia can cause ventricular tachycardia (VT) in patients with structurally normal heart. Contrary to the fact that in patients with chronic myocardial scarring the ventricular tachycardia is monomorphic, in patients with acute ischemia the ventricular tachycardia is polymorphic and is reversible with coronary revascularization.
We are reporting a 40 year old male who presented with recurrent syncope due to polymorphic ventricular tachycardia in the context of normal QT interval in baseline ECG and normal left ventricular function without any evidence of myocardial injury. Due to recurrent fatal ventricular arrhythmia despite medical management, urgent coronary angiography was done which showed critical obstruction of right coronary artery (RCA). Considering the critical obstruction of RCA responsible for polymorphic VT, emergency PCI of RCA was done. After successful PTCA and stenting to RCA, he had another episode of polymorphic VT which was terminated with intravenous phenytoin. Seven days after the PCI, 24 hours Holter monitoring was done which showed normal sinus rhythm with infrequent ventricular premature complexes and no evidence of VT. He was asymptomatic at six months follow-up.
Acute coronary ischemia; Polymorphic VT
Hyperkalemia is a common condition, particularly in the setting of renal dysfunction. Hyperkalemia due to intentional oral potassium overdose is not commonly reported.
We present a case of acute intentional potassium overdose in a patient with normal renal function resulting in significant hyperkalemia, with a maximum serum potassium concentration of 11 mEq/L. Despite an initial course complicated by various unstable cardiac rhythms, including ventricular tachycardia, ventricular fibrillation, and pulseless electrical activity, the patient was discharged from the hospital neurologically intact. Treatment for hyperkalemia included hemodialysis.
The role of dialysis in potassium overdose is poorly defined.
Based on this case and a review of the medical literature, we recommend hemodialysis for cases of potassium overdose with hemodynamic instability and significantly elevated serum potassium concentrations that do not respond promptly to medical therapy. Hemodialysis should also be considered in cases with underlying renal dysfunction.
Hyperkalemia; Potassium; Overdose; Dialysis
Trandolapril is a well known angiotensin converting enzyme (ACE) inhibitor with many cardiovascular (CV) indications. The objectives of this article are to review the pharmacokinetics and pharmacodynamics properties of trandolapril and to focus on its clinical relevance in cardiovascular medicine. Various populations have been studied in large clinical trials including patients with congestive heart failure (CHF) after an acute myocardial infarction (AMI), diabetics, patients with hypertension (HTN), stable coronary artery disease (CAD) and prevention of proteinuria. Long-term treatment with trandolapril in patients with reduced left ventricular function soon after AMI significantly reduced the risk of overall mortality, mortality from CV causes, sudden death, and the development of severe CHF. Treatment with trandolapril after AMI complicated by left ventricular dysfunction appears to be of considerable importance in patients with diabetes mellitus by saving lives and substantially reducing the risk of progression to severe CHF as well. Moreover, trandolapril reduces progression to proteinuria in high-risk patients. Some of the advantages of trandolapril over other ACE inhibitors are the wide spectrum of patient populations studied, the well established dosage and its proven trough-to-peak effect ratios permitting a safe once-a-day administration.
trandolapril; angiotensin converting enzyme inhibitors; hypertension cardiovascular diseases; diabetic nephropathy
Intractable ventricular tachyarrhythmia associated with hypomagnesemia responds well to magnesium given intravenously. Two patients with recurrent ventricular tachycardia and ventricular fibrillation associated with normal serum magnesium levels and resistant to treatment with potassium chloride, lidocaine and bretylium tosylate responded dramatically to the administration of magnesium sulfate. A third patient in whom the serum magnesium level was unknown also showed dramatic response to magnesium therapy.
Magnesium depletion probably interferes with sodium-potassium adenosine triphosphatase enzyme activity and causes ionic imbalance and electrical instability of purkinje's fibers. Without obvious magnesium depletion this element in high concentration may still prolong transient inward current, prolong the effective refractory period, increase the membrane potential and control ventricular tachyarrhythmia.
When ventricular fibrillation or malignant ventricular tachycardia cannot be controlled with lidocaine and other conventional drugs, we recommend infusing magnesium sulfate, 2 to 3 grams in one minute, followed by 10 grams over five hours.
To study whether emergent intracoronary autologous bone marrow cell transplantation (BMT) is applicable for the treatment of acute myocardial infarction (AMI).
20 patients admitted within 24 h after the onset of a first AMI were randomly allocated to receive intracoronary autologous BMT (n = 10) or bone marrow supernatant (controls, n = 10) immediately after primary percutaneous coronary intervention. Left ventricular ejection fraction (LVEF), left ventricular end diastolic internal diameter (LVDd) and myocardial perfusion defect scores were examined respectively by echocardiography and single‐photon emission computed tomography at one week and six months after AMI.
From one week to six months after AMI, LVEF was enhanced from mean 53.8 (SD 9.2)% to 58.6 (9.9)% (p < 0.05) in the BMT group but was unchanged in the control group (58.2 (7.5)% v 56.3 (3.5)%, p > 0.05); LVDd remained unchanged (52.5 (2.8) v 52.1 (3.2) mm, p > 0.05) in the BMT group but was significantly enlarged in the control group (50.4 (6.0) v 55.2 (7.1) mm, p < 0.05). Additionally, myocardial perfusion defect scores decreased from 21 (11) to 13 (10) (p < 0.01) in the BMT group but were unchanged in the control group (20 (14) v 17 (15), p > 0.05).
Emergent intracoronary transplantation of bone marrow mononuclear cells after AMI is practicable, and it improved cardiac function, prevented myocardial remodelling and increased myocardial perfusion at six months' follow up.
The purpose of this study was to compare cardiovascular magnetic resonance (CMR) and echocardiography (echo) in patients treated with primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) with emphasis on the analysis of left ventricular function and left ventricular wall motion characteristics.
We performed CMR and echo in 52 patients with first AMI shortly after primary angioplasty and four months thereafter. CMR included cine-MR and T1-weighted first-pass and late-gadolinium enhancement (LGE) sequences. Global ejection fraction (EFCMR, %) and regional left ventricular function (systolic wall thickening %, [SWT]) were determined from cine-MR images. In echo the global left ventricular function (EFecho, %) and regional wall motion abnormalities were determined. A segment in echo was scored as "infarcted" if it was visually > 50% hypokinetic.
EFecho revealed a poor significant agreement with EFCMR at baseline (r: 0.326; p < 0.01) but higher correlation at follow-up (r: 0.479; p < 0.001). The number of infarcted segments in echocardiography correlated best with the number of segments which showed systolic wall thickening < 30% (r: 0.498; p < 0.001) at baseline and (r: 0.474; p < 0.001) at follow-up. Improvement of EF was detected in both CMR and echocardiography increasing from 44.2 ± 11.6% to 49.2 ± 11% (p < 0.001) by CMR and from 51.2 ± 8.1% to 54.5 ± 8.3% (p < 0.001) by echocardiography.
Wall motion and EF by CMR and echocardiography correlate poorly in the acute stage of myocardial infarction. Correlation improves after four months. Systolic wall thickening by CMR < 30% indicates an infarcted segment with influence on the left ventricular function.