Aditya S. Bharadwaj

Healthy Eating Index and mortality in a nationally representative elderly cohort.

was associated with a 28% lower risk of death even after these factors, as well as depression and health behaviors, had been taken into account. Other factors may be responsible for the remaining association between enjoyment and survival. It may be caused by unmeasured confounding factors such as other pre-existing illnesses. Only 3 health behaviors were assessed, and other aspects such as diet may be relevant. In addition, direct links with health outcomes are plausible, since biological responses such as reduced cortisol output in everyday life and attenuated cardiovascular and inflammatory responses to stress are related to positive well-being. The results of this study do not establish that enjoyment of life is causally related to survival. Enjoyment may be a marker of underlying health-related biological, behavioral, or dispositional factors that are responsible for the association. Nonetheless, our findings show that the link between enjoyment and survival at older ages is not fully accounted for by demographic factors or major preexisting illnesses. These results highlight the importance of positive well-being in older adults and suggest that efforts to improve enjoyment of life, as well to manage and prevent disease, could have beneficial effects on life expectancy.

Prognostic Importance of Defibrillator Shocks in Survivors of Sudden Cardiac Death

Implantable cardioverter-de fi brillator (ICD) implantation is standard of care for patients who have survived life threatening ventricular tachyarrhythmias (LTVA). ICD shocks predict future adverse events in patients with ICD implantation for primary prevention. However, the role of ICD shocks in prediction of adverse events in a secondary prevention population is unknown. The Antiarrhythmics Versus ICDs (AVID) Trial (n=1016) was a randomized controlled trial comparing ICD (n=507) and antiarrhythmic drugs (n=509) in the treatment of patients with LTVA. Mean follow-up duration was 916 ± 471 days. We analyzed the ICD arm of the AVID trial using the NHLBI limited access dataset. ICD shocks were categorized as appropriate if underlying rhythm triggering the shock was ventricular tachycardia or ventricular fibrillation. All other ICD shocks were considered as inappropriate. Data on ICD therapy was available for 420 patients. Any shock (n=380), any appropriate (n=296) or any inappropriate (n=72) shock was not associated with increased all cause, cardiac or arrhythmic mortality. However any appropriate shock was associated with increased LTVA. In conclusion, ICD shocks do not confer increased risk of death on follow up in LTVA survivors. Use of ICD shocks as surrogate marker for adverse outcomes is not viable in secondary prevention patients.

Outcomes and Risk Prediction Model for Peripheral Arterial Disease in Patients with Stable Coronary Artery Disease

We used the National Heart, Lung, and Blood Institute Limited Access Dataset of Prevention of Events with Angiotensin-Converting Enzyme Inhibition (PEACE) Trial (n = 8290) which included patients with stable coronary artery disease (CAD) and preserved ejection fraction (>40%). We identified risk factors for the development of critical peripheral arterial disease (PAD; those needing angioplasty, bypass grafting, or aneurysm repair) and formulated a risk score by multivariate analyses. A total of 220 patients (2.8%) developed critical PAD over a mean follow-up of 4.7 years. Significant predictors of critical PAD were history of intermittent claudication, smoking, hypertension (HTN), coronary-artery bypass grafting (CABG), diabetes, age, serum cholesterol, and body mass index (BMI). Incident critical PAD was associated with increased composite outcome of cardiovascular death, myocardial infarction, percutaneous transluminal coronary angioplasty, or CABG (hazard ratio 1.82, 95% CI 1.50-2.22, P < .001). Risk assessment using our score may identify CAD patients at risk for critical PAD events.

Combined use of direct renin inhibitor and carvedilol in heart failure with preserved systolic function

HYPOTHESES Heart failure with preserved systolic function (HFPSF) has attained epidemic proportions; however evidence-based therapeutic interventions have not advanced despite continued research over the past three decades. We propose the combined use of direct renin inhibitor and carvedilol for this condition. RATIONALE The Renin Angiotensin Aldosterone System (RAAS) plays a central role in myocyte hypertrophy, fibrosis and ventricular remodeling which is responsible for the diastolic dysfunction in HFPSF. Rising serum aldosterone levels with age have been implicated as a cause of myocardial fibrosis in the elderly. The sole use of Angiotensin Converting Enzyme Inhibitors or Angiotensin Receptor Blockers is associated with angiotensin-II and aldosterone escape and increased plasma renin activity. Carvedilol is a novel third generation non-selective β-blocker. The use of combination therapy will facilitate in better blood pressure control, reduce afterload, improve ventricular relaxation, cause regression of ventricular remodeling/fibrosis, maintain atrioventricular synchrony and enhance cardio-metabolic profile. The individual benefits of direct renin inhibitor and carvedilol could plausibly have a supra-additive effect when used in combination. Besides this, carvedilol can further reduce generation of free radicals, decrease LDL oxidation, improve Doppler echo diastolic parameters and decrease cardiac norepinephrine and density of cardiac β-receptors. CONCLUSION Evidence suggests that patients with HFPSF are treated less aggressively as compared to patients with heart failure with systolic dysfunction. Aggressive therapy with concurrent use of direct renin inhibitor and carvedilol will help in improving outcomes in this vulnerable patient sub-population. No prior trial has evaluated the combined use of these drugs for the treatment of HFPSF.

‘UnSTEADy'ness in elderly: Unexplained syncope induced by tachycardia in elderly with AV nodal disease and LV diastolic dysfunction

Syncope is most often due to temporary and self-terminating global cerebral hypoperfusion with an increased incidence in patients older than 70 years of age [1]. Although the etiopathogenesis of syncope is largely ascribed to neurally mediated, cardiovascular and orthostatic mechanisms, around 18% of patients have multiple potential causes, sometimes overlapping or by hitherto unexplained mechanisms [2]. Herein, we present a case of unexplained syncope and elucidate a mechanism which could plausibly explain the etiopathogenesis in a subset of elderly population presenting with syncope. An 84-year old Caucasian woman was brought to our emergency department (ED) after she passed out while watching and cheering at a baseball game. The patient was apparently pulseless at that time according to a family friend cardiologist who was seated next to her and had performed cardiopulmonary resuscitation. In the ED, her vital signs were stable with no orthostatic intolerance and the physical exam was unremarkable. Her past medical history included hypertension, gastroesophageal reflux disease and two recent episodes of

Preserved or slightly depressed ejection fraction and outcomes after myocardial infarction

Background Left ventricular ejection fraction (EF) in post-myocardial infarction (MI) patients is a strong predictor of adverse cardiovascular events. Although resting EF as measured by transthoracic echocardiography (TTE), contrast ventriculography (CNV), and radionuclide angiography (RNA) exhibit high correlation, there is only modest agreement between these modalities. This study sought to explore whether modality of EF assessment influences prognostication of post-MI patients with normal or slightly reduced EF. Methods and results The National Heart, Lung, and Blood Institute (NHLBI) limited access dataset of the Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) Trial (1996–2003, n=8290) comparing trandolapril versus placebo was used. The cohort was partitioned into TTE (n=2582), RNA (n=816), and CNV (n=1155) groups based on modality of EF assessment. EF was a significant predictor of cardiovascular mortality (HR 0.97, 95% CI 0.95 to 0.98; p<0.005) and all cause mortality (HR 0.98, 95% CI 0.97 to 0.99; p=0.0002) on multivariate analysis in this population with preserved or mildly depressed EF. Although CNV, TTE, and RNA groups differed significantly in terms of baseline variables, no appreciable differences were noted between RNA (HR 1.13, 95% CI 0.85 to 1.50; ns) and CNV (HR 1.13, 95% CI 0.99 to 1.27; ns) groups, compared with TTE for all cause mortality. Similarly, no significant differences were observed for cardiovascular mortality between RNA (HR 1.23, 95% CI 0.82 to 1.84; p=0.31) and CNV (HR 1.14, 95% CI 0.78 to 1.67, p=0.49) versus TTE. Conclusion EF is a significant predictor of all-cause mortality and cardiovascular mortality in patients with preserved or mildly depressed EF. Modalities of EF measurement are interchangeable and do not play a significant role in prognostication in a post-MI population.

VACCINATION SEROLOGY STATUS (NON-PNEUMOCOCCAL AND NON-INFLUENZA) AND CARDIOVASCULAR MORTALITY: INSIGHTS FROM NHANES III

Methods: The public dataset of the National Health and Nutrition Examination Survey III (NHANES III) between the years 1988-1994 was used. We included patients >18 years with data on antibody titres for tetanus, measles, rubella or diphtheria (n= 6776). Protective titers were analyzed as >0.10IU/ml, >0.15IU/ml and ≥10U for diphtheria, tetanus and mumps respectively per standard protocols. Univariate and multivariate analyses were carried out using SAS 9.1. Baseline differences in traditional cardiovascular risk factors, CRP and insurance status were adjusted in the multivariate Cox proportional hazard regression. Two separate models were analyzed using immune status. First model included immune status as continuous variable (0, 1, 2, 3 or 4). The second model analyzed immune status as positive for two or more vaccinations versus none or single positive titer.