Background: Self-reported family history of cardiovascular disease (CVD) is an independent risk factor for future coronary heart disease (CHD) events. However, inclusion of family history of CVD in the traditional risk scores failed to improve risk prediction of CHD. It is proposed that family history of CVD may substantially increase the risk of CHD among younger individuals. Methods: We conducted a matched case-control study with 170 hospital-based premature CHD patients (<55 years in men and <65 years in women) from a tertiary care centre in Thiruvananthapuram, Kerala and age and sex matched community-based controls in 1:1 ratio. Conditional logistic regression analysis was conducted to assess the independent association of family history of cardiovascular disease (CVD) and premature CHD. We estimated McNemar's odds ratios and their 95 percent confidence intervals. Results: The prevalence of any family history of CVD and CHD in the control population was 24% and 21%, respectively. The family history of CVD was independently associated with premature CHD (odds ratio (OR) = 9.0; 95% confidence interval (CI) 4.7–17.3). There was a dose-response relationship between family history and premature CHD as the risk increased linearly with increase in number of affected family members. Conclusions: Family history of CVD is an independent risk factor for premature CHD. The risk of premature CHD increases linearly with increase in number of affected family members. Collecting family history beyond parental history of CVD is important for risk stratification. Targeting young individuals with family history of CVD for intensive risk reduction interventions may help to prevent future events.
Objective Heart failure (HF) has emerged as a global public health problem that affects both low and high-income countries. The high HF burden and the need for resource-intensive treatments often lead to health system crisis in resource-poor settings. Data on prevailing practice patterns and long-term clinical outcomes of HF are scarce from the low and middle-income countries. Nationally representative HF data from India are not available. Methods The National Heart Failure Registry (NHFR) is a multicentric, hospital-based registry of HF patients from 53 centers across India. Consecutive patients admitted with the diagnosis of acute decompensated HF satisfying the European Society of Cardiology (ESC) 2016 criteria will be enrolled into the registry from January 2019 to December 2019. Each participating center is expected to contribute 200 patients into the registry (i.e., more than 10,000 HF patients from India). We are collecting demographics, clinical, laboratory, imaging, and other diagnostic data at baseline from all registered patients in the registry by using a structured document. Additionally, we are collecting the details of treatment practices and the usage of guideline-directed therapy from all participants. We intend to obtain the in-hospital, 3-months, 6-months and one-year outcome data on mortality, cause of death, and repeated hospitalization events. Conclusions In summary, NFHR will be the first nationally representative HF registry aimed at providing crucial information on prevailing etiology, distribution and current practices in the management of HF.
Background: Self-reported family history of cardiovascular disease (CVD) is an independent risk factor for future coronary heart disease (CHD) events. However, inclusion of family history of CVD in the traditional risk scores failed to improve risk prediction of CHD. It is proposed that family history of CVD may substantially increase the risk of CHD among younger individuals. Methods: We conducted a matched case-control study with 170 hospital-based premature CHD patients (<55 years in men and <65 years in women) from a tertiary care centre in Thiruvananthapuram, Kerala and age and sex matched community-based controls in 1:1 ratio. Conditional logistic regression analysis was conducted to assess the independent association of family history of cardiovascular disease (CVD) and premature CHD. We estimated McNemar's odds ratios and their 95 percent confidence intervals. Results: The prevalence of any family history of CVD and CHD in the control population was 24% and 21%, respectively. The family history of CVD was independently associated with premature CHD (odds ratio (OR) = 9.0; 95% confidence interval (CI) 4.7–17.3). There was a dose-response relationship between family history and premature CHD as the risk increased linearly with increase in number of affected family members. Conclusions: Family history of CVD is an independent risk factor for premature CHD. The risk of premature CHD increases linearly with increase in number of affected family members. Collecting family history beyond parental history of CVD is important for risk stratification. Targeting young individuals with family history of CVD for intensive risk reduction interventions may help to prevent future events.
A community-based cross-sectional study was undertaken by the Cardiology Society of India (Kerala Chapter) to determine the prevalence of coronary artery disease (CAD) and its risk factors. The periodontal health status of the rural and urban participants in the Thiruvananthapuram district of Kerala was evaluated to document any association between periodontal disease (PD) and CAD and to describe any shared risk factors. The participants were selected using a multistage cluster random sampling method. Socio-demographic data and personal histories were collected using a structured interview schedule and validated tools. Body mass index, blood pressure, electrocardiogram, and biochemical investigations were recorded and analyzed using standard protocols. A modification of the Ramfjord periodontal disease index was used to assess periodontal health. PD was more frequent among rural (61.4%) than in the urban population (35.5%). The frequencies of CAD associated with PD in the rural and urban populations were 82.6% and 40.5%, respectively. PD was not found to be a significant risk factor for CAD in the univariate regression analysis of urban populations. In the rural population, the odds of PD as a risk factor for CAD were found to be 3.08 (95% CI [1.38–8.38]) and significant ( P = .043) in univariate regression analysis and 1.54 (95% CI: 0.44–5.4) and non-significant ( P = .503) in the multivariate regression analysis. In rural areas, male sex and dyslipidemia demonstrated borderline significance as risk factors for CAD. PD was not found to be an independent risk factor after adjusting for age, sex, tobacco use, hypertension, sedentary lifestyle, and dyslipidemia. Male sex and dyslipidemia were identified as shared risk factors between PD and CAD, which could have confounded the significant association between the latter. In urban areas, age, male sex, and dyslipidemia demonstrated an independent association with CAD. This study could not establish an independent association between PD and CAD in either community. Future epidemiological studies should identify and recruit novel environmental factors to understand the interrelationships between PD and CAD and focus on the role of effect modifiers that may have a protective role against PD colluding with CAD.
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