Determinants Of Sudden Cardiac Death Research Articles

Extreme Risk of Sudden Cardiac Death within Three Months after Revascularization in Patients with Ischemic Left Ventricular Systolic Dysfunction.

The risk of sudden cardiac death (SCD) after coronary revascularization in patients with left ventricular (LV) systolic dysfunction has not been characterized completely. This study aims to evaluate the incidence and time course of SCD after revascularization in such patients. The determinants of SCD within 3 months after revascularization were also assessed. A cohort study of patients with reduced ejection fraction (EF 40%), who underwent revascularization was performed. The incidence of SCD was estimated to account for the competing risk of deaths due to other causes. 2317 patients were enrolled. With a median follow-up of 3.5 years, 162 (32.1%) of the 504 deaths were due to SCD. The risk of SCD was highest in the first 3 months after revascularization, with an incidence rate of 0.37%/month. The event rate decreased to 0.12%/month, 0.08%/month, 0.09%/month, 0.14%/month, and 0.19%/month at 3-6 months, 6-12 months, 1-3 years, 3-5 years, and 5-10 years, respectively. A history of ventricular tachycardia/ventricular fibrillation (hazard ratio [HR], 5.55; 95% confidence interval [CI], 1.33-23.19; p = 0.019) and triple vessel disease (HR, 3.90; 95% CI, 1.38-11.05; p = 0.010) were associated with the risk of SCD within 3 months. However, preoperative EF (in 5% increments) was not predictive (HR per 5% increase, 0.98; 95% CI, 0.62-1.55; p = 0.935). For patients with LV dysfunction, the risk of SCD was the highest during the first 3 months after revascularization. Further risk classification and treatment strategy are warranted. The name of the registry: Coronary Revascularization in Patients with Ischemic Heart Failure and Prevention of Sudden Cardiac Death. Registration number: ChiCTR2100044378.

Sudden cardiac death after heart transplantation: a population-based study.

The epidemiology of sudden cardiac death (SCD) after heart transplantation (HTx) remains imprecisely described. We aimed to assess the incidence and determinants of SCD in a large cohort of HTx recipients, compared with the general population. Consecutive HTx recipients (n = 1246, 2 centres) transplanted between 2004 and 2016 were included. We prospectively assessed clinical, biological, pathologic, and functional parameters. SCD was centrally adjudicated. We compared the SCD incidence beyond the first year post-transplant in this cohort with that observed in the general population of the same geographic area (registry carried out by the same group of investigators; n = 19 706 SCD). We performed a competing risk multivariate Cox model to identify variables associated with SCD. The annual incidence of SCD was 12.5 per 1,000 person-years [95% confidence interval (CI), 9.7-15.9] in the HTx recipients cohort compared with 0.54 per 1,000 person-years (95% CI, 0.53-0.55) in the general population (P < 0.001). The risk of SCD was markedly elevated among the youngest HTx recipients with standardized mortality ratios for SCD up to 837 for recipients ≤30 years. Beyond the first year, SCD was the leading cause of death. Five variables were independently associated with SCD: older donor age (P = 0.003), younger recipient age (P = 0.001) and ethnicity (P = 0.034), pre-existing donor-specific antibodies (P = 0.009), and last left ventricular ejection fraction (P = 0.048). HTx recipients, particularly the youngest, were at very high risk of SCD compared with the general population. The consideration of specific risk factors may help identify high-risk subgroups.

Abstract 10541: Clinical Risk Factors and Myocardial Fibrosis in Subjects Who Died Suddenly: Pilot Data from A 10-Year Post-Mortem Data Registry

Introduction: Sudden cardiac death (SCD) is responsible for approximately 380,000 deaths per year. One third of the patients dying of heart disease present with SCD as the first manifestation. There are limited data on the clinico-pathological determinants of SCD. Hypothesis: We hypothesized that, compared to overall deaths, silent coronary atherosclerosis and myocardial fibrosis could be associated with increased frequency of SCDs. Methods: We reviewed the post-mortem data registry from two tertiary care hospitals located at the Buffalo-Niagara Region. Of the 1,314 subjects that underwent comprehensive post-mortem analysis, we identified 187 subjects that died suddenly. For this initial pilot data analysis protocol, we compared the demographic, clinical, electrocardiographic and coronary vascular and myocardial histopathological characteristics of 109 subjects with sudden death vs. 34 age-matched controls with non-sudden death. Results: We found that, of the total 1,314 subjects screened, 14% had SCD. Comparison of age-matched SCD with non-SCD subjects (age in years, SCD: 60±14; non-SCD: 61±20) showed that SCD groups had larger cardiac size (heart weight in grams, SCD: 550±150; non-SCD: 480±117, P=0.03), increased wall thickness (posterior wall thickness in cm, SCD: 1.7±0.4; non-SCD: 1.5±0.2, P=0.01), but reduced LV function reported before the event (LV ejection fraction in %, SCD: 41±17; non-SCD: 58±9, P=0.007). In addition, SCD groups had higher frequency of coronary atherosclerosis (SCD, 76% vs., non-SCD, 52%, P=0.007), and myocardial fibrosis involving both left ventricular free wall (SCD, 47% vs., non-SCD, 26%, P=0.03), and interventricular septum (SCD, 29% vs., non-SCD, 3%, P=0.02). There were no differences on serum electrolytes, circulating biomarkers and the extent of right ventricular fibrosis. Conclusions: The subjects that died suddenly had larger cardiac size, reduced contractile function with myocardial interstitial fibrosis, and silent coronary atherosclerosis. Further studies are in progress to fully examine the clinico-pathological correlates of SCD in our longitudinal study cohorts.

Cholesterol lowering, sudden cardiac death and mortality

Sudden cardiac death is the main cause of cardiac mortality. Is blood cholesterol a determinant of sudden cardiac death? Does cholesterol lowering result in fewer sudden cardiac deaths? Answering these two questions may shed a new light on the epidemiology of coronary heart disease and on prevention options. In fact, careful analysis of the available data, including randomised trials, indicates that, contrary to a widespread opinion, cholesterol lowering does not appear to be a very effective way of reducing cardiac and overall mortality in the general population.

Cholesterol lowering and mortality: Time for a new paradigm?

Sudden cardiac death is the main cause of cardiac mortality. Is blood cholesterol a determinant of sudden cardiac death? Does cholesterol lowering result in fewer sudden cardiac deaths? Answering these two questions may shed new light on the epidemiology of coronary heart disease and on prevention options. In fact, careful analysis of the available data, including randomised trials, indicates that, contrary to a widespread opinion, cholesterol lowering does not appear to be a very effective way of reducing cardiac and overall mortality in the general population.

Determinants of sudden cardiac death in individuals with the electrocardiographic pattern of brugada syndrome and no previous cardiac arrest

Background— Patients with Brugada syndrome who were resuscitated from an episode of ventricular fibrillation are at high risk for recurrent sudden death. There is general agreement about the therapeutic strategy for these patients. Conversely, the prognosis and approach in patients with a diagnostic ECG but without a previous history of sudden cardiac death is controversial. We analyzed a large cohort of patients with Brugada syndrome without previous cardiac arrest to understand the determinants of prognosis. Methods and Results— A total of 547 patients with an ECG diagnostic of Brugada syndrome and no previous cardiac arrest were studied. The mean age was 41±15 years, and 408 were male. The diagnostic ECG was present spontaneously in 391 patients. In the remaining 156 individuals, the abnormal ECG was noted only after the administration of an antiarrhythmic drug. One hundred twenty-four patients had suffered from at least 1 episode of syncope. During programmed ventricular stimulation, a sustained ventr...

Prospective study of sudden cardiac death among women in the United States.

There are few data regarding the determinants of sudden cardiac death (SCD) in women, primarily because of their markedly lower rate of SCD compared with men. Nonetheless, existing data, although sparse, suggest possible gender differences in risk factors for SCD. In this prospective cohort of 121 701 women aged 30 to 55 years at baseline, SCD was defined as death within 1 hour of symptom onset. From 1976 to 1998, 244 SCDs were identified. Although the risk of SCD increased markedly with age, the percentage of cardiac deaths that were sudden decreased. Most (69%) women who suffered a SCD had no history of cardiac disease before their death. However, almost all of the women who died suddenly (94%) had reported at least 1 coronary heart disease risk factor. Smoking, hypertension, and diabetes conferred markedly elevated (2.5- to 4.0-fold) risk of SCD, similar to that conferred by a history of nonfatal myocardial infarction (relative risk, 4.1; 95% confidence interval, 2.9 to 6.7). Family history of myocardial infarction before age 60 years and obesity were associated with moderate (1.6-fold) elevations in risk. With regard to mechanism, 88% of SCDs were classified as arrhythmic. In 76% of these, the first rhythm documented was ventricular tachycardia or ventricular fibrillation. These prospective data suggest that, as in men, coronary heart disease risk factors predict risk of SCD in women and that SCD is usually an arrhythmic death. Therefore, prevention of atherosclerosis or ventricular arrhythmias may reduce the incidence of SCD in women.

3693 Determinants of sudden cardiac death in patients with the electrocardiographic pattern of brugada syndrome

3693 Determinants of sudden cardiac death in patients with the electrocardiographic pattern of brugada syndrome

Sickle Cell Trait and Sudden Death in Athletes-Reply

In Reply. —Drs Kerle and Runkle have made a reasonable point regarding the potential role that sickle cell trait may have played in the sudden deaths of young African-American athletes with cardiovascular disease in our study population. As Kerle and Runkle point out, sickle cell trait has been incriminated as a sole determinant of sudden cardiac death with exertion,1,2and indeed, 1 of our athletes without a detectable cardiac abnormality had only the finding of sickle trait to explain sudden death. Among the 134 competitive athletes in our study, we found hypertrophic cardiomyopathy to be the most common cause of sudden death. Of the 48 athletes assigned this diagnosis at autopsy, the majority were black. Unfortunately, our study design did not include a systematic analysis for sickle cell trait in these individuals. Also, we encountered 14 other athletes who showed an increase in left ventricular mass, but no other features of

Influence of spontaneous hypertension and cardiac hypertrophy on the severity of ischemic arrhythmias in the rat.

Cardiac hypertrophy (CH) and hypertension (HT) are major determinants of sudden cardiac death in patients with coronary artery disease. To investigate the hypothesis that CH and HT increase the incidence of severe ventricular arrhythmias in an animal model, we performed a 30-min period of coronary artery ligation in anesthetized spontaneously hypertensive rats (SHR), normotensive Wistar Kyoto (WKY) and Wistar (W) rats. The incidence and duration of ventricular fibrillation resulting from coronary artery occlusion were significantly (p less than 0.01) increased in hypertensive rats compared to normotensive animals. The calcium entry blocker nicardipine was administered orally to SHR either chronically for 8 weeks (20 mg.kg-1 twice daily) or acutely as a single dose of 20 mg.kg-1. After long-term treatment with nicardipine, left ventricular hypertrophy index and systolic blood pressure were significantly (p less than 0.001) reduced when compared to vehicle-treated SHR, whereas a single administration of nicardipine only decreased blood pressure without affecting cardiac mass. In the long-term nicardipine-treated SHR group, acute coronary artery ligation induced significantly less ventricular fibrillation (p less than 0.05) and mortality (p less than 0.001) than in acutely nicardipine-treated or untreated SHR groups. In conclusion, the data suggest that the severity and incidence of lethal ventricular arrhythmias are more elevated in hypertensive than in normotensive rats and this may be related to the myocardial hypertrophic state.