During the past 30 years, Portugal has been described as one of the countries with highest median blood pressure levels in Europe, but the incidence of hypertension is unknown. The aim of this study was to estimate the incidence of hypertension, according to socio-demographic characteristics and lifestyles.
A population-based cohort of randomly selected dwellers from Porto, Portugal, aged ≥18 years, was assembled in 1999–2003 (EPIPorto study) and 796 hypertension-free individuals (62.6% women) were reassessed after a median of 3.8 years. Hypertension was defined as blood pressure ≥140/90 mmHg and/or antihypertensive drug therapy. Incidence rate ratios (IRR) were estimated using Poisson regression.
The overall incidence rate was 47.3 [95% confidence interval (95% CI): 40.5-55.5] per 1000 person-years. Among women, the incidence was 43.4 (35.6-53.1) and among men 52.7 (41.3-68.0) per 1000 person-years. The incidence was lower in women up to 60 years and much higher among women above 60 (110.0 vs. 64.4 per 1000 person-years among men, p for age-sex interaction=0.032). Participants with higher education had a lower risk of becoming hypertensive (≥13 years vs. ≤4 years: RR=0.70, 95% CI, 0.46-1.08, p for linear trend <0.001), independently of age and sex. Overweight and obesity were associated with a 1.67-fold and 2.44-fold increased risk of hypertension, respectively, independently of age, sex and education.
In this urban Portuguese population the incidence rate of hypertension was high, with new cases occurring predominantly among older subjects, the less educated and those with overweight-obesity. Despite recent progresses in blood pressure related outcomes, the risk of hypertension remains higher in Portugal than in other developed countries.
Adults; Hypertension; Incidence; Portugal
In Australia, rheumatic heart disease (RHD) is almost exclusively restricted to Aboriginal Australian and Torres Strait Islander people with children being at highest risk. International criteria for echocardiographic diagnosis of RHD have been developed but the significance of minor heart valve abnormalities which do not reach these criteria remains unclear. The Rheumatic Fever Follow-Up Study (RhFFUS) aims to clarify this question in children and adolescents at high risk of RHD.
RhFFUS is a cohort study of Aboriginal and/or Torres Strait Islander children and adolescents aged 8–17 years residing in 32 remote Australian communities. Cases are people with non-specific heart valve abnormalities detected on prior screening echocardiography. Controls (two per case) are age, gender, community and ethnicity-matched to cases and had a prior normal screening echocardiogram. Participants will have echocardiography about 3 years after initial screening echocardiogram and enhanced surveillance for any history suggestive of acute rheumatic fever (ARF). It will then be determined if cases are at higher risk of (1) ARF or (2) developing progressive echocardiography-detected valve changes consistent with RHD.
The occurrence and timing of episodes of ARF will be assessed retrospectively for 5 years from the time of the RhFFUS echocardiogram. Episodes of ARF will be identified through regional surveillance and notification databases, carer/subject interviews, primary healthcare history reviews, and hospital separation diagnoses.
Progression of valvular abnormalities will be assessed prospectively using transthoracic echocardiography and standardized operating and reporting procedures. Progression of valve lesions will be determined by specialist cardiologist readers who will assess the initial screening and subsequent RhFFUS screening echocardiogram for each participant. The readers will be blinded to the initial assessment and temporal order of the two echocardiograms.
RhFFUS will determine if subtle changes on echocardiography represent the earliest changes of RHD or mere variations of normal heart anatomy. In turn it will inform criteria to be used in determining whether secondary antibiotic prophylaxis should be utilized in individuals with no clear history of ARF and minor abnormalities on echocardiography. RhFFUS will also inform the ongoing debate regarding the potential role of screening echocardiography for the detection of RHD in this setting.
Rheumatic heart disease; Acute rheumatic fever; Screening; Aboriginal; Torres Strait Islander; Indigenous; Diagnosis; Prevention; Australia; Echocardiography
Radiofrequency catheter ablation (RFCA) has been used for the ablation of premature ventricular contractions (PVCs) or ventricular tachycardia (VT). To date, the mapping and catheter ablation of the arrhythmias originating from the left ventricular outflow tract (LVOT) has not been specified. This study investigates the electrocardiogram (ECG) feature of PVCs or VT originating from the LVOT. Moreover, the treatment outcome of RFCA is analyzed.
Mapping and ablation were performed on the supravalvular or subvalvular aorta in 52 cases with PVCs/VT originating from the LVOT. The data were compared with those from 104 patients with PVCs/VT originating from the right ventricular outflow tract (RVOT). A differential procedure was prepared based on the comparison of the ECG features of PVCs/VT originating from the RVOT, LVOT, and their different parts.
Among 52 cases with PVCs originating from the LVOT, 47 were successfully treated by RFCA, with a success rate of 90.38%. Several differences among the 12-lead ECG features were observed from the RVOT and LVOT in the left and right coronary sinus groups, as well as under the left coronary sinus group (left fibrous trigone): (1) If the precordial leads transition 0 are considered as the diagnostic parameters of PVCs/VT originating from the LVOT, then the sensitivity, specificity, as well as positive and negative predictive values are 94.12%, 93.00%, 87.27%, and 96.88%, respectively; (2) The analysis of different subgroups of the LVOT are as follows: (a) A mainly positive wave of r or m pattern was recorded in the lead I in 72.73% of patients in the right coronary sinus group, versus 12.90% of patients in the left coronary sinus group, and 0% in the under left coronary sinus group. (b) All patients in the right coronary sinus group presented waves of RII>RIII and QSaVR>QSaVL, whereas most patients in the other two groups showed waves of RIII>RII and QSaVL>QSaVR. (c) Most patients in the under left coronary sinus group in lead V1 had a mainly positive wave (R) (77.78%), whereas those in the right (81.82%) and left (62.50%) coronary sinus groups had mainly negative waves (rS).
RFCA is a safe and effective curative therapy for PVCs/VT originating from the LVOT. The 12-lead ECG features of the LVOT from different origins exhibit certain distinctions.
Electrophysiology; Ventricular arrhythmia; Left ventricular outflow; Catheter ablation; Radiofrequency current
New-onset atrial fibrillation in patients hospitalized for an acute myocardial infarction often leads to hemodynamic deterioration and has serious adverse prognostic implications; mortality is particularly high in patients with congestive heart failure and/or a reduced left ventricular ejection fraction. The mechanism of atrial fibrillation in the context of an acute myocardial infarction has not been well characterized and an effective treatment other than optimal medical therapy and mechanical hemodynamic support are expected.
A 71 year-old male with an acute myocardial infarction due to an occlusion of the left main coronary artery was treated with percutaneous coronary intervention. He had developed severe congestive heart failure with a left ventricular ejection fraction of 34%. The systemic circulation was maintained with an intraaortic balloon pump, continuous hemodiafiltration, and mechanical ventilation until atrial fibrillation occurred on day 3 which immediately led to cardiogenic shock. Because atrial fibrillation was refractory to intravenous amiodarone, beta-blockers, and a total of 15 electrical cardioversions, the patient underwent emergent radiofrequency catheter ablation on day 4. Soon after electrical cardioversion, ectopies from the right superior pulmonary vein triggered the initiation of atrial fibrillation. The right pulmonary veins were isolated during atrial fibrillation. Again, atrial fibrillation was electrically cardioverted, then, sinus rhythm was restored. Subsequently, the left pulmonary veins were isolated. The stabilization of the hemodynamics was successfully achieved with an increase in the blood pressure and urine volume. Hemodiafiltration and amiodarone were discontinued. The patient had been free from atrial fibrillation recurrence until he suddenly died due to ventricular fibrillation on day 9.
To the best of our knowledge, this is the first report of pulmonary vein isolation for a rescue purpose applied in a patient with hemodymically unstable atrial fibrillation complicated with an acute myocardial infarction. This case demonstrates that ectopic activity in the pulmonary veins may be responsible for triggering atrial fibrillation in the critical setting of an acute myocardial infarction and thus pulmonary vein isolation could be an effective therapeutic option.
Atrial fibrillation; Acute myocardial infarction; Cardiogenic shock; Catheter ablation; Congestive heart failure; Pulmonary vein isolation
With hypertension, the cardiovascular system changes to adapt to the varying neuro-humoral and hemodynamic changes and this may lead to the development of different left ventricular geometric patterns, each carrying a different risk profile for major adverse cardiovascular events.
Using a consecutive sampling technique, a cross-sectional, prospective, hospital based study was done and two hundred and twenty seven (227) hypertensive patients were studied.
The distribution of different abnormal LV geometrical patterns was 19.8%, 28.2%, 22% for concentric remodelling, concentric hypertrophy and eccentric hypertrophy respectively. With echocardiographic criteria, the proportion of patients with left ventricular hypertrophy (LVH) was higher when left ventricular mass (LVM) was indexed to height2.7 than to body surface area (70.0% vs. 52.9%). Duration of hypertension markedly influenced the type of LV geometry with normal LV geometry predominating in early hypertension and abnormal geometrical patterns predominating in late hypertension. The left ventricular fractional shortening decreased with duration of hypertension and was common in patients with eccentric hypertrophy. Age of the patient, systolic blood pressure, duration of hypertension and body mass index were found to be independent predictors left ventricular hypertrophy.
About 70% of hypertensive patients had abnormal geometry existing in different patterns. Eccentric hypertrophy had more of clinical and echocardiographic features suggestive of reduced left ventricular systolic function. Hypertensive patients should be recognized as a heterogeneous population and therefore stratifying them into their respective LV geometrical patterns is useful as way of assessing their risk profile as well as instituting appropriate management.
Echocardiography; Essential hypertension; Left ventricular hypertrophy; Left ventricular geometry; Left ventricular mass index; Left ventricular function
Atrial fibrillation (AF) is the most common sustained arrhythmia observed in clinical practice. Electrical cardioversion (EC) is commonly used to restore and maintain sinus rhythm but it is characterized by high rate of recurrences. Several trials analyzed the effects of statins to reduce the recurrences in AF with contradictory results.
We performed a meta-analysis of the interventional trials with statins in patients with persistent AF to evaluate recurrences after EC. Only randomized controlled trials were included in the analysis. Data sources included: Medline, ISI Web of Science, SCOPUS and Cochrane database (up to June 2012). Data extraction was performed by three authors. Study-specific odds ratios (ORs) were combined using fixed-effects model.
Six studies with 515 patients were included in the analysis. Statins used in the selected trials were: atorvastatin (at dosages ranging from 10 to 80 mg/day), pravastatin (40 mg/day) and rosuvastatin (20 mg/day). AF recurrence after EC occurred in 108/258 (41.8%) of patients treated with statins and in 132/257 (51.3%) patients not on treatment with statins. Compared with control, recurrences were significantly reduced with statin treatment (O.R.: 0.662; 95% C.I., 0.45-0.96; p=0.03); statin treatment was associated with an absolute risk reduction of 0.095 and a number needed to treat of 11.
This review suggests that statin therapy was significantly associated with a decreased risk of recurrence in patients with persistent AF after EC.
Atrial fibrillation; Statin; Electrical cardioversion
Limited data are available on the risk ratios for fatal cardiovascular disease (CVD) outcome from gout and chronic kidney disease (CKD) in non-diabetic individuals.
Nationwide population-based retrospective prospective study with a 5-year follow-up to investigate the association between physician-diagnosed gout and CKD in non-diabetics aged 50 and above who had no pre-existing serious CVD and the subsequent risk of death from CVD. Hazard ratios (HR) of CVD mortality were adjusted for gender, age, smoking- and alcoholism-related diagnoses, hypertension, hyperlipidemia, atrial fibrillation and Charlson’s comorbidity index score.
A case cohort (n=164,463) having gout and a control cohort (n= 3,694,377) having no gout were formed. The prevalence of gout in this study was 4.26% whereas that of gout plus CKD was 8.17%. Male to female ratio among the individuals with gout was 3.2:1. The relative risk (RR) of subsequent cardiovascular mortality between the case and control cohort was 1.71 (95% confidence interval (CI), 1.66-1.75). The presence of CKD in nondiabetic subjects with no gout (control group) has a RR of CVD mortality at 3.05 (95% CI, 2.94-3.15). The presence of gout has protective effect on subjects with CKD with a RR of 1.84 (95% CI, 1.71-1.98). As compared with individuals with no gout, the adjusted HR (aHR) for CVD mortality among the individuals with gout was 1.10 (95% CI 1.07-1.13). In a Cox model, when compared with subjects having neither gout nor CKD, the aHR in subjects with no gout but with CKD is 1.76 (95% CI, 1.70-1.82); in subjects with gout but without CKD, 1.10 (1.07-1.13); interestingly, the aHR is attenuated in subjects with concomitant gout plus CKD which is 1.38 (1.29-1.48).
Among non-diabetic individuals aged 50 years or above who had no preceding serious CVD, those with gout were 1.1 times more likely to die from CVD as were individuals without gout. The presence of gout appears to attenuate the risk of subsequent CV mortality in subjects with CKD. Further studies should focus on finding an explanation for the protective effect of gout on CV mortality in patients with CKD.
There has been a paucity of autopsy studies on atherosclerotic lesions in Nigerians, the last one conducted at our centre being more than four decades ago. There has also been considerable epidemiological transition. The objective of the study was to determine the frequency, severity, pattern and distribution of atherosclerotic lesions in extra cranial carotid arteries (ECCA) in Nigerians at autopsy.
ECCA of 30 consecutive Nigerian patients undergoing autopsy at a University teaching hospital were examined using the American Heart Association (AHA) histological grading and classification of atherosclerosis.
Atherosclerotic lesions of ECCA were present in 73.3% of the subjects with the right and the left carotid bifurcations (28.3%) being the most frequently affected sites. Using the AHA classification of atherosclerosis, a total of 176(73.3%) lesions were found in the 240 histological sections of blood vessels examined. Of these, 22.5% were types I, 22.5% were types II, 15.4% were type V, and 7.5% were type III. The VII to type IX lesions were rare. When these atherosclerotic lesions were grouped into mild, moderate and severe, 52.5% were mild lesions (types I-III); 18.3% were moderate lesions (types IV and V); and 2.5% were severe lesions (types VI to IX). The severe lesions were most frequently observed in the left carotid bifurcation (50%) and they first appeared in the age group 45–49 years. Age, hypertension and diabetes mellitus were strong risk factors for atherosclerosis.
Compared with four decades ago there has been an apparent increase in severity and extent of ECCA atherosclerosis especially after the age of 45 years in autopsies from our centre. This change in the amount of atherosclerosis over time is possibly due to the epidemiologic transition. This may worsen the rise in stoke incidence within this community and as such, great effort should be made to follow-up and manage CVD risk factors within the community.
Extra cranial atherosclerosis; Plaques; Nigerians; Autopsy; Cardiovascular risk factors
Infective Endocarditis (IE) is considered as a multifaceted problem in every aspect from etiology and presentation to diagnosis and management. Early recognition of this disease and especially its complications, remain a critical task for the cardiologist. Atrial endocarditis is a rare and sometimes unrecognized complication of mitral valve endocarditis.
We present a 48 year-old male patient who was admitted to our clinic because of recent onset of malaise, fever, jaundice and peripheral edema. Important physical findings were peripheral stigmata of IE in addition to holosystolic murmur over the left sternal border. Transthoracic and transesophageal echocardiophy revealed a severe eccentric MR due to a flailed posterior mitral valve caused by IE. The presence of atrial septal endocarditis caused by jet streaming was also observed. Blood culture was positive for streptococcus oralis and antibiotic therapy was immediately initiated. Considering the large burden of infective tissue, the patient was planned for an early surgical intervention. A minimally invasive resection of the atrial mass, direct closure of the defect, resection of the diseased portions of mitral leaflets and implantation of a biological mitral valve prosthesis was performed. Intra-operative and histological findings confirmed provisional diagnosis by echocardiography.
Together with comprehensive echocardiographic evaluation, attention should be placed on mural vegetations and excluded among all cases of mitral valve endocarditis, particularly those with severe eccentric regurgitant jets.
It’s unknown whether the prognostic value of admission heart rate (HR) was different in patients with ST-segment elevation myocardial infarction (STEMI) with or without concomitant type 2 diabetes mellitus (T2DM).
Consecutive STEMI patients who presented within 12 hours of symptom onset were recruited from 274 hospitals in China. Participants were stratified into quartiles by admission HR. Baseline characteristics, current therapeutic recommenda- tions, laboratory biochemical tests, 30-day all-cause mortality and Cardiovascular Events (CVE, including all-cause death, reinfarction and stroke) were compared across admission HR quartiles.
We evaluated 7294 STEMI patients, of these 820 (11.2%) had known T2DM. The admission HR quartile stratification was significantly associated with all-cause mortality and CVE regardless of T2DM status (P < 0.001 both for survival and CVE). After adjusted other risk factors, in patients without T2DM, comparing with HR <66 b.p.m., the increase of HR level was associated with worse prognosis (P < 0.05). In patients with T2DM, the hazard ratios for 30-day CVE were 1.75 (95%CI), 1.92 (95%CI), 3.00 (95%CI) in the HR of 66–76 b.p.m., 77–88 b.p.m., and >88 b.p.m., respectively. Results were similar for 30-day all-cause mortality, but the hazard ratios in Q2 (P = 0.139 and P =0.086 for survival and CVE, respectively) and Q3 groups were non-significant (P = 0.072 and P =0.033 for survival and CVE, respectively). There was a significant interaction effect of HR and T2DM on 30-day CVE mortality (P = 0.035), which was not found on all-cause mortality (P = 0.126).
Admission heart rate was an important risk factor of 30-day all-cause mortality and CVE in patients with STEMI with or without T2DM. However, the predictive effect was modified by T2DM.
Heart rate; ST-segment elevation myocardial infarction; Type 2 Diabetes Mellitus; Prognosis
We evaluated the association between linear standard Heart Rate Variability (HRV) measures and vascular, renal and cardiac target organ damage (TOD).
A retrospective analysis was performed including 200 patients registered in the Regione Campania network (aged 62.4 ± 12, male 64%). HRV analysis was performed by 24-h holter ECG. Renal damage was assessed by estimated glomerular filtration rate (eGFR), vascular damage by carotid intima-media thickness (IMT), and cardiac damage by left ventricular mass index.
Significantly lower values of the ratio of low to high frequency power (LF/HF) were found in the patients with moderate or severe eGFR (p-value < 0.001). Similarly, depressed values of indexes of the overall autonomic modulation on heart were found in patients with plaque compared to those with a normal IMT (p-value <0.05). These associations remained significant after adjustment for other factors known to contribute to the development of target organ damage, such as age. Moreover, depressed LF/HF was found also in patients with left ventricular hypertrophy but this association was not significant after adjustment for other factors.
Depressed HRV appeared to be associated with vascular and renal TOD, suggesting the involvement of autonomic imbalance in the TOD. However, as the mechanisms by which abnormal autonomic balance may lead to TOD, and, particularly, to renal organ damage are not clearly known, further prospective studies with longitudinal design are needed to determine the association between HRV and the development of TOD.
Heart Rate Variability; Target organ damage; Hypertension
Type VI dual left anterior descending artery (LAD) is a rare coronary anomaly, the first case of which has recently been described. This is the first report of type VI dual LAD anomaly in which the patient presented with non-ST-segment elevation myocardial infarction and percutaneous coronary intervention was performed in the anomalously originating LAD.
A 52-year-old man with diabetes, hypertension and hyperlipidemia presented with chest pain without ST elevation on EKG, although the patient’s troponin I level was elevated. Coronary angiography revealed a short LAD originating from the left main coronary artery and a long LAD originating from the proximal portion of the right coronary artery (RCA). Three-dimensional reconstruction of computed tomography of images revealed that the long LAD originated from the proximal RCA and coursed between the right ventricular outflow tract (RVOT) and the aortic root before entering the mid anterior interventricular groove. The high take-off RCA originated underneath the RVOT, pointing downwards and forming an acute angle with the proximal portion of the long LAD. The anomalous long LAD displayed significant stenosis. We performed successful percutaneous coronary intervention (PCI) in the anomalous artery.
With accurate understanding of the coronary anatomy and appropriate hardware selection, successful PCI can be performed in the in the long LAD in patients with type VI dual LAD anomaly.
Type VI dual LAD anomaly; Percutaneous coronary intervention; Computed tomographic coronary angiography
We aimed to evaluate the multivariate association between functional microvascular variables and clinical-laboratorial-anthropometrical measurements.
Data from 189 female subjects (34.0±15.5 years, 30.5±7.1 kg/m2), who were non-smokers, non-regular drug users, without a history of diabetes and/or hypertension, were analyzed by principal component analysis (PCA). PCA is a classical multivariate exploratory tool because it highlights common variation between variables allowing inferences about possible biological meaning of associations between them, without pre-establishing cause-effect relationships. In total, 15 variables were used for PCA: body mass index (BMI), waist circumference, systolic and diastolic blood pressure (BP), fasting plasma glucose, levels of total cholesterol, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), triglycerides (TG), insulin, C-reactive protein (CRP), and functional microvascular variables measured by nailfold videocapillaroscopy. Nailfold videocapillaroscopy was used for direct visualization of nutritive capillaries, assessing functional capillary density, red blood cell velocity (RBCV) at rest and peak after 1 min of arterial occlusion (RBCVmax), and the time taken to reach RBCVmax (TRBCVmax).
A total of 35% of subjects had metabolic syndrome, 77% were overweight/obese, and 9.5% had impaired fasting glucose. PCA was able to recognize that functional microvascular variables and clinical-laboratorial-anthropometrical measurements had a similar variation. The first five principal components explained most of the intrinsic variation of the data. For example, principal component 1 was associated with BMI, waist circumference, systolic BP, diastolic BP, insulin, TG, CRP, and TRBCVmax varying in the same way. Principal component 1 also showed a strong association among HDL-c, RBCV, and RBCVmax, but in the opposite way. Principal component 3 was associated only with microvascular variables in the same way (functional capillary density, RBCV and RBCVmax). Fasting plasma glucose appeared to be related to principal component 4 and did not show any association with microvascular reactivity.
In non-diabetic female subjects, a multivariate scenario of associations between classic clinical variables strictly related to obesity and metabolic syndrome suggests a significant relationship between these diseases and microvascular reactivity.
Microcirculation; Capillaries; Obesity; Metabolic syndrome; Impaired fasting glucose; Principal component analysis
This study was performed to investigate the relationship between elastic properties of aorta and left atrium volume index (LAVI) in hemodialyzed (HD) patients.
Study group was consisted of 73 patients (age 51,6 ± 7,6 years) treated by hemodialysis. In all patients standard echocardiography was performed. Aortic stiffness index (ASI) was calculated using formula: ASI = log (SBP/DBP)/[(Aomax-Aomin)/Aomin]. LAVI was calculated according to the formula: LAVI = [π/6 x (LAmax x LAshort x LAlong)]/m2. Additionally several indices were calculated: left ventricle mass (LVM), left ventricle mass index (LVMI), midwall fractional shortening (mFS), endsystolic stress (ESS), mFS/ESS. Additionally the laboratory parameters including lipidogram, troponin T (cTnT), NT-proBNP and asymmetric dimethylarginine (ADMA) were measured.
The ASI was strong and significantly correlated with left atrium volume (LAV) and LAVI (respectively: 0,601; p < 0,001 and 0,598; p < 0,001). The ASI was independently and markedly associated with ADMA, cTnT, CRP, T-chol, and LDL-chol. The LAVI was independently and significantly correlated with NT-proBNP and cTnT.
There is correlation between ASI and ADMA, marker of endothelium dysfunction. There is also association between LAVI and NT-proBNP, signs of elevated left atrium pressure. The strong correlation between ASI and LAVI, improved by associations of specific biochemical markers with these echocardiographic indices, suggests there is the link between elastic properties of aorta and left atrium pressure in hemodialysed patients mediated by endothelial dysfunction.
Left atrium volume index; Aortic stiffness; NT-pro BNP; Asymmetric dimethylarginine; End-stage renal disease; Hemodialysis
Cardiovascular diseases contribute substantially to the poor health and reduced life expectancy of Indigenous Australians. Heart failure is a common, disabling, progressive and costly complication of these disorders. The epidemiology of heart failure and the adequacy of relevant health service provision in Indigenous Australians are not well delineated.
A systematic search of the electronic databases PubMed, Embase, Web of Science, Cinahl Plus, Informit and Google Scholar was undertaken in April 2012 for peer-reviewed journal articles relevant to the topic of heart failure in Indigenous Australians. Additionally, a website search was done to identify other pertinent publications, particularly government reports.
There was a paucity of relevant peer-reviewed research, and government reports dominated the results. Ten journal articles, 1 published conference abstract and 10 reports were eligible for inclusion. Indigenous Australians reportedly have higher morbidity and mortality from heart failure than their non-Indigenous counterparts (age-standardised prevalence ratio 1.7; age-standardised hospital separation ratio ≥3; crude per capita hospital expenditure ratio 1.58; age-adjusted mortality ratio >2). Despite the evident disproportionate burden of heart failure in Indigenous Australians, the accuracy of estimation from administrative data is limited by poor indigenous identification, inadequate case ascertainment and exclusion of younger subjects from mortality statistics. A recent journal article specifically documented a high prevalence of heart failure in Central Australian Aboriginal adults (5.3%), noting frequent undiagnosed disease. One study examined barriers to health service provision for Indigenous Australians in the context of heart failure.
Despite the shortcomings of available published data, it is clear that Indigenous Australians have an excess burden of heart failure. Emerging data suggest that undiagnosed cases may be common in this population. In order to optimise management and to inform policy, high quality research on heart failure in Indigenous Australians is required to delineate accurate epidemiological indicators and to appraise health service provision.
Heart failure; Australia; Indigenous; Aboriginal; Torres Strait Islander; Cardiac failure; Cardiovascular; Heart disease
In Poland, the prevalence of cardiovascular diseases is increasing. This might be associated with the constantly growing proportion of elderly people and inappropriate cardiovascular prevention. This study aimed to evaluate the frequency of use of oral antiplatelet (OAP) and oral anticoagulant (OAC) drugs among older people in Poland and to assess their association with cardiovascular risk factors.
The study was based on data collected during the implementation of a multicentre, publicly funded research project called PolSenior.
The study group consisted of 4,979 people with the average age of 79.35 ± 8.69 years. Among them, 1,787 people (35.9%) used at least one drug in the prevention of cardiovascular diseases. OAPs were used regularly by 1,648 (33.1%) elderly people and OACs were used by 165 elderly people (3.3%). Acetylsalicylic acid was used by 32.2% of elderly people. Use of drugs significantly depended on age (p < 0.01), sex (p < 0.01), place of residence (p < 0.001), level of education (p < 0.0001) and personal income (p < 0.0001). Among all the respondents treated with OAPs, therapy was applied as secondary cardiovascular prevention in 717 respondents (43.5%), and as primary prevention in 705 respondents (42.8%). Among the respondents treated with OACs, 117 (71%) elderly people had a history of atrial fibrillation. Secondary cardiovascular prevention should be considered in a further 482 respondents (15.1% of untreated elderly people), and primary cardiovascular prevention in 1,447 respondents (45.3%).
Our study is the first to determine the frequency of use of OAP and OAC drugs among elderly people in Poland in relation to cardiovascular risk factors. The most commonly used drug for cardiovascular prevention is acetylsalicylic acid, but it appears that it is used too rarely in high-risk patients. Educational programs should be developed among general practitioners concerning current recommendations for pharmacological cardiovascular prevention.
Epidemiology; Elderly; Public health; Preventive medicine; Oral anticoagulant drugs; Antiplatelet drugs; Acetylsalicylic acid
Heart failure is a major cause of mortality and morbidity. As mortality rates are high, it is important that patients seen by general practitioners with symptoms suggestive of heart failure are identified quickly and treated appropriately. Identifying patients with heart failure or deciding which patients need further tests is a challenge. All patients with suspected heart failure should be diagnosed using objective tests such as echocardiography, but it is expensive, often delayed, and limited by the significant skill shortage of trained echocardiographers. Alternative approaches for diagnosing heart failure are currently limited. Clinical decision tools that combine clinical signs, symptoms or patient characteristics are designed to be used to support clinical decision-making and validated according to strict methodological procedures. The REFER Study aims to determine the accuracy and cost-effectiveness of our previously derived novel, simple clinical decision rule, a natriuretic peptide assay, or their combination, in the triage for referral for echocardiography of symptomatic adult patients who present in general practice with symptoms suggestive of heart failure.
This is a prospective, Phase II observational, diagnostic validation study of a clinical decision rule, natriuretic peptides or their combination, for diagnosing heart failure in primary care. Consecutive adult primary care patients 55 years of age or over presenting to their general practitioner with a chief complaint of recent new onset shortness of breath, lethargy or peripheral ankle oedema of over 48 hours duration, with no obvious recurrent, acute or self-limiting cause will be enrolled. Our reference standard is based upon a three step expert specialist consensus using echocardiography and clinical variables and tests.
Our clinical decision rule offers a potential solution to the diagnostic challenge of providing a timely and accurate diagnosis of heart failure in primary care. Study results will provide an evidence-base from which to develop heart failure care pathway recommendations and may be useful in standardising care. If demonstrated to be effective, the clinical decision rule will be of interest to researchers, policy makers and general practitioners worldwide.
Heart failure; Clinical decision rule; Diagnosis; Echocardiogram; NT-proBNP
Circulating endothelial progenitor cells (EPCs) capture technology improves endothelialization rates of sirolimus-eluting stents (SES), but the problem of delayed re-endothelialization, as well as endothelial dysfunction, has still not been overcome. Therefore, we investigated whether the combination coating of hyaluronan-chitosan (HC) and anti-CD34 antibody applied on an SES (HCASES) can promote endothelialization, while reducing neointimal formation and inflammation.
Sirolimus-eluting stents(SES), anti-CD34 antibody stents (GS) and HC-anti-CD34 antibody combined with sirolimus-eluting stents (HCASES) were deployed in 54 normal porcine arteries and harvested for scanning electron microscopy (SEM) and histological analysis. The ratio of endothelial coverage above the stents was evaluated by SEM analysis at 7, 14 and 28 days. The percentage of in-stent stenosis was histologically analyzed at 14 and 28 days.
SEM analysis at 7 days showed that endothelial strut coverage was increased in the HCASES group (68±7%) compared with that in the SES group (31±4%, p=0.02). At 14 days, stent surface endothelialization, evaluated by SEM, showed a significantly higher extent of endothelial coverage above struts in the GS (95 ± 2%) and the HCASES groups (87±4%) compared with that in the SES group (51±6%, p=0.02). Histological examination showed that the percentage of stenosis in the HCASES group was not significantly different to that of the SES and GS groups (both p> 0.05). At 28 days, there was no difference in the rates of endothelial coverage between the HCASES and GS groups. The HCASES group showed less stenosis than that in the GS group (P < 0.05), but it was not significantly different from the SES group (P=0.068).
SEM and histology demonstrated that HCASESs can promote re-endothelialization while enhancing antiproliferative effects.
Anti-CD34 antibody; Endothelial progenitor cells; Hyaluronan and chitosan coating; Scanning electron microscopy
Long QT syndrome (LQTS) is an inherited arrhythmic disorder characterised by prolongation of the QT interval on ECG, presence of syncope and sudden death. The symptoms in LQTS patients are highly variable, and genotype influences the clinical course. This study aims to report the spectrum of LQTS mutations in a Swedish cohort.
Between March 2006 and October 2009, two hundred, unrelated index cases were referred to the Department of Clinical Genetics, Umeå University Hospital, Sweden, for LQTS genetic testing. We scanned five of the LQTS-susceptibility genes (KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2) for mutations by DHPLC and/or sequencing. We applied MLPA to detect large deletions or duplications in the KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes. Furthermore, the gene RYR2 was screened in 36 selected LQTS genotype-negative patients to detect cases with the clinically overlapping disease catecholaminergic polymorphic ventricular tachycardia (CPVT).
In total, a disease-causing mutation was identified in 103 of the 200 (52%) index cases. Of these, altered exon copy numbers in the KCNH2 gene accounted for 2% of the mutations, whereas a RYR2 mutation accounted for 3% of the mutations. The genotype-positive cases stemmed from 64 distinct mutations, of which 28% were novel to this cohort. The majority of the distinct mutations were found in a single case (80%), whereas 20% of the mutations were observed more than once. Two founder mutations, KCNQ1 p.Y111C and KCNQ1 p.R518*, accounted for 25% of the genotype-positive index cases. Genetic cascade screening of 481 relatives to the 103 index cases with an identified mutation revealed 41% mutation carriers who were at risk of cardiac events such as syncope or sudden unexpected death.
In this cohort of Swedish index cases with suspected LQTS, a disease-causing mutation was identified in 52% of the referred patients. Copy number variations explained 2% of the mutations and 3 of 36 selected cases (8%) harboured a mutation in the RYR2 gene. The mutation panorama is characterised by founder mutations (25%), even so, this cohort increases the amount of known LQTS-associated mutations, as approximately one-third (28%) of the detected mutations were unique.
Arrhythmia; Long QT syndrome; Ion-channel; Founder mutation; Variant of unknown significance
Nonsteroidal anti-inflammatory drugs (NSAIDs) may disrupt control of blood pressure in hypertensive patients and increase their risk of morbidity, mortality, and the costs of care. The objective of this study was to examine the association between incident use of NSAIDs and blood pressure in patients with hypertension.
We conducted a retrospective cohort study of adult hypertensive patients to determine the effects of their first prescription for NSAID on systolic blood pressure and antihypertensive drug intensification. Data were collected from an electronic medical record serving an academic general medicine practice in Indianapolis, Indiana, USA. Using propensity scores to minimize bias, we matched a cohort of 1,340 users of NSAIDs with 1,340 users of acetaminophen. Propensity score models included covariates likely to affect blood pressure or the use of NSAIDs. The study outcomes were the mean systolic blood pressure measurement after starting NSAIDs and changes in antihypertensive therapy.
Compared to patients using acetaminophen, NSAID users had a 2 mmHg increase in systolic blood pressure (95% CI, 0.7 to 3.3). Ibuprofen was associated with a 3 mmHg increase in systolic blood pressure compared to naproxen (95% CI, 0.5 to 4.6), and a 5 mmHg increase compared to celecoxib (95% CI, 0.4 to 10). The systolic blood pressure increase was 3 mmHg in a subgroup of patients concomitantly prescribed angiotensin converting enzyme inhibitors or calcium channel blockers and 6 mmHg among those prescribed a beta-adrenergic blocker. Blood pressure changes in patients prescribed diuretics or multiple antihypertensives were not statistically significant.
Compared to acetaminophen, incident use of NSAIDs, particularly ibuprofen, is associated with a small increase in systolic blood pressure in hypertensive patients. Effects in patients prescribed diuretics or multiple antihypertensives are negligible.
NSAIDs; Hypertension; Blood pressure; Propensity score
Areca nut (commonly known as betel nut) chewing has been shown to be associated with metabolic syndrome and cardiovascular disease (CVD). The mechanism by which betel nut ingestion could lead to development of CVD is not precisely known; however, dyslipidemia, hyperhomocysteinemia, hypertriglyceridemia and inflammation could be some of the potential risk factors. This study was undertaken to investigate the effects of two dosages of betel nut on homocysteinemia, inflammation and some of the components of metabolic syndrome, such as hypertriglyceridemia, low HDL-cholesterol, obesity and fasting hyperglycemia in a rat model.
Thirty-six adult female Sprague Dawley rats, aged 10–12 weeks were divided into three equal groups. Group-1 served as the control group (n = 12) and received water, whereas groups 2 and 3 were given water suspension of betel nut orally in two dosages, 30 mg and 60 mg, respectively for a period of 5 weeks. At the end of the fifth week, the animals were weighed and sacrificed, blood was collected and liver, kidney, spleen and stomach were removed for histological examination.
Plasma/serum was analyzed for glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, homocysteine, folate, vitamin B12 and N-acetyl-β-D-glucosaminidase (NAG) – a marker of inflammation.
When the mean concentration values of 3 groups were compared using one way ANOVA followed by Tukey’s HSD-test, there was a significant increase in the concentration of total cholesterol (p = 0.04) in the group receiving 30 mg/day betel nut compared to the control group. However, administration of a higher dose of betel nut (60 mg/day) had no significant effect on the serum concentrations of glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol, and NAG. Histological examination of spleen revealed a dose-dependent extramedullary hematopoiesis. No other remarkable change in the tissues (liver, kidney and stomach) was observed.
Mean serum/plasma levels of folate, vitamin B12 and homocysteine were not found to be significantly different in all the groups. Betel nut ingestion had no effect on the mean body weights of rats.
Low dosage of betel nut is found to be associated with hypercholesterolemia. However, betel nut ingestion is not associated with hyperhomocysteinemia, hypertriglyceridemia, hyperglycemia, inflammation and increase in body weight in a rat model.
Areca nut; Betel nut; Cardiovascular disease; Metabolic syndrome; Rat model
There is limited information about any association between the onset of atrial fibrillation (AF) and the presence of valvular disease.
We retrospectively examined 940 patients in sinus rhythm, examined by echocardiography in 1996. During 11 years of follow-up, we assessed the incidence of AF and outcome defined as valvular surgery or death, in relation to baseline valvular function. AS (aortic stenosis) severity at baseline examination was assessed using peak transaortic valve pressure gradient.
In univariate analysis, the risk of developing AF was related to AS (significant AS versus no significant AS; hazard ratio (HR) 3.73, 95% confidence interval (CI) 2.39-5.61, p<0.0001) and mitral regurgitation (MR) (significant MR versus no significant MR; HR 2.52, 95% CI 1.77-3.51, p<0.0001). Also the risk of valvular surgery or death was related to AS (HR 3.90, 95% CI 3.09-4.88, p<0.0001) and MR (HR 2.07, 95% CI 1.67-2.53, p<0.0001). In multivariate analyses, adjusting for sex, age, other valvular abnormalities, left ventricular ejection fraction and left atrial size − AS was independently related to both endpoints, whereas MR was not independently related to either endpoint.
AS, but not MR, was independently predictive of development of AF and combined valvular surgery or death. In patients with combined AS and MR, the grade of AS, more than the grade of MR, determined the risk of AF and combination of valvular surgery or death. Further studies using contemporary echocardiographic quantification of aortic stenosis are warranted to confirm these retrospective data based on peak transaortic valve pressure gradient.
Atrial fibrillation; Aortic stenosis; Mitral regurgitation; Valvular heart disease; Remodelling
Neointimal formation in atherosclerosis has been subject for intense research. However, good animal models mimicking asymmetrical lesion formation in human subjects have been difficult to establish. The aim of this study was to develop a model which would lead to the formation of eccentric lesions under macroscopically intact non-denuded endothelium.
We have developed a new collar model where we placed two cushions or dots inside the collar. Arterial lesions were characterized using histology and ultrasound methods.
When this dotted collar was placed around carotid and femoral arteries it produced asymmetrical pressure on adventitia and a mild flow disturbance, and hence a change in shear stress. Our hypothesis was that this simple procedure would reproducibly produce asymmetrical lesions without any intraluminal manipulations. Intima/media ratio increased towards the distal end of the collar with the direction of blood flow under macroscopically intact endothelium. Macrophages preferentially accumulated in areas of the thickest neointima thus resembling early steps in human atherosclerotic plaque formation. Proliferating cells in these lesions and underlying media were scarce at eight weeks time point.
The improved dotted collar model produces asymmetrical human-like atherosclerotic lesions in rabbits. This model should be useful in studies regarding the pathogenesis and formation of eccentric atherosclerotic lesions.
Atherosclerotic lesion; Carotid collar; Rabbit; Shear stress
Genetic variation at 1p13 modulates serum lipid levels and the risk of coronary heart disease through the regulation of serum lipid levels. Here we investigate if the interaction between genetic variants at 1p13 and serum lipid levels affects the risk of non-fatal myocardial infarction (MI) in the Stockholm Heart Epidemiology Program (SHEEP), a large population based case control study.
In the present study only non fatal MI cases (n = 1213, men/women: 852/361) and controls (n = 1516, men/women =1054/507) matched by age, sex and residential area, were included. Three SNPs 12740374 G/T, rs599839A/G and rs646776T/C mapping at 1p13 were analysed for association with serum lipid levels and the risk of MI by a weighted least square regression and logistic regression analyses, respectively. To analyse the effect of the interaction between genetic variants and serum lipid levels on the risk of MI, we applied the biological model of interaction that estimates the difference in risk, expressed as OR (95%CI), observed in the presence and in the absence of both exposures. One derived measure is the Synergy index (S) and 95%CI, where S > 1 indicates synergy and S < 1 antagonism between the two interaction terms.
Rs12740374G/T and rs646776T/C were in strong linkage disequilibrium (LD) (r2 = 0.99), therefore only rs599839A/G and rs646776 were included in the analysis. Consistently with published data, presence of the rare genotypes was associated with reduced total-, LDL-cholesterol and ApoB serum levels (all p < 0.05) as compared to the reference genotype, but was not associated with the risk of MI.
However, the increased risk of MI observed in individual exposed to high (≥75th percentile) serum lipid levels was offset in subjects carrying the rare alleles G and C. In particular, the risk of MI associated with high ApoB serum levels OR (95%CI) 2.27 (1.86-2.77) was reduced to 1.76 (1.33-2.34) in the presence of the G allele at rs599839 with an S of 0.47 (0.20-0.90).
These results indicate that an antagonism between ApoB serum levels and genetic variants at 1p13 contributes to reduce the risk of non-fatal MI in the presence of high ApoB serum levels.
Patients with Senning repair for complete transposition of the great arteries (d-TGA) show an impaired exercise tolerance. Our aim was to investigate changes in exercise capacity in children, adolescents and adults with Senning operation.
Peak oxygen uptake (peak VO2), oxygen pulse and heart rate were assessed by cardiopulmonary exercise tests (CPET) and compared to normal values. Rates of change were calculated by linear regression analysis. Right ventricular (RV) function was assessed by echocardiography.
Thirty-four patients (22 male) performed 3.5 (range 3–6) CPET with an interval of ≥ 6 months. Mean age at first assessment was 16.4 ± 4.27 years. Follow-up period averaged 6.8 ± 2 years. Exercise capacity was reduced (p<0.0005) and the decline of peak VO2 (−1.3 ± 3.7 %/year; p=0.015) and peak oxygen pulse (−1.4 ± 3.0 %/year; p=0.011) was larger than normal, especially before adulthood and in female patients (p<0.01). During adulthood, RV contractility changes were significantly correlated with the decline of peak oxygen pulse (r= −0.504; p=0.047).
In patients with Senning operation for d-TGA, peak VO2 and peak oxygen pulse decrease faster with age compared to healthy controls. This decline is most obvious during childhood and adolescence, and suggests the inability to increase stroke volume to the same extent as healthy peers during growth. Peak VO2 and peak oxygen pulse remain relatively stable during early adulthood. However, when RV contractility decreases, a faster decline in peak oxygen pulse is observed.
Exercise capacity; Transposition of the great arteries; Senning repair; Median term follow-up