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The association between familial occurrence of atrial fibrillation (AF) and new-onset AF beyond established risk factors is determined. The studies have shown that familial AF is associated with an increased risk of AF that is not attenuated by adjustment for AF risk factors including genetic variants.

A study was conducted to investigate and identify genetic variants that are associated with cardiac structure and function through a meta-analysis. Results indicated that there were 5 genetic loci, associated with variance in cardiac dimensions and aortic root size; however, the proportion of variance is quite small.

A study was conducted to evaluate the importance and clinical significance of prolonged PR interval in ambulatory individuals. Results indicated that prolonged PR interval led to an increased risk of incident atrial fibrillation (AF), pacemaker implantation as well as mortality.

The relationship between pulse pressure and incident atrial fibrillation (AF) is examined. The results have shown that the pulse pressure is an important risk factor for incident AF in a community-based sample.

Stepwise logistic regression was used to determine the impact of risk factors on the occurrence of new-onset kidney disease. It was found that onset of new kidney disease is associated with cardiovascular disease risk factors.

The risk of stroke in patients with atrial fibrillation depends on their age, blood pressure, history of diabetes, heart disease or a previous stroke, and whether they smoke. Doctors can assign points to all of these values and then determine an individual patient's risk of having a stroke. Patients with a high risk can take anticoagulant drugs if necessary.

Measuring blood levels of natriuretic peptides does not appear to be useful as a screening tool for detecting people who have a precursor of heart disease called left ventricular hypertrophy. In a study of 3,177 people, only one-third who had left ventricular hypertrophy on an echocardiogram were identified by the blood test. Natriuretic peptides are produced when the heart is damaged.

The lifetime risk of developing high blood pressure in middle and old age is about 90%, according to a study of 1,298 people participating in the Framingham Heart Study. However, the lifetime risk of developing severe hypertension is much lower, most likely due to effective treatments., Context The long-term risk for developing hypertension is best described by the lifetime risk statistic. The lifetime risk for hypertension and trends in this risk over time are unknown. Objectives To estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk. Design, Setting, and Participants Community-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998). Main Outcome Measures Residual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications. Results The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher ([greater than or equal to]140/90 mm Hg regardless of treatment) were 90% in both 55-and 65-year-old participants. The lifetime probability of receiving antihypertensive medication was 60%. The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period. In contrast, the residual lifetime risk for stage 2 high blood pressure or higher ([greater than or equal to]160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure. Conclusion The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden. Although the decline in lifetime risk for stage 2 high blood pressure or higher represents a major achievement, efforts should be directed at the primary prevention of hypertension.

Chronic hypertension appears to be a strong risk factor for congestive heart failure (CHF). Researchers followed 5,143 men and women participating in the Framingham Heart Study and the Framingham Offspring Study for up to 20 years. Half of the participants had hypertension at the start of the study. During the study, 392 participants developed CHF. Ninety-one percent had hypertension at the start of the study. Eighty-two percent of the female CHF patients and 76% of the male CHF patients had stage 2 hypertension at the start of the study. Men with hypertension at the start of the study had twice the risk of CHF and women with hypertension had three times the risk. Half of the men and one-third of the women had a history of heart attack at the start of the study. Diabetes, enlargement of the left ventricle of the heart and heart valve disease at the start of the study also increased the risk of developing CHF., Objectives. - To study the relative and population-attributable risks of hypertension for the development of congestive heart failure (CHF), to assess the time course of progression from hypertension to CHF, and to identify risk factors that contribute to the development of overt heart failure in hypertensive subjects. Design. - Inception cohort study. Setting. - General community. Participants. - Original Framingham Heart Study and Framingham Offspring Study participants aged 40 to 89 years and free of CHF. To reflect more contemporary experience, the starting point of this study was January 1, 1970. Exposure Measures. - Hypertension (blood pressure of at least 140 mm Hg systolic or 90 mm Hg diastolic or current use of medications for treatment of high blood pressure) and other potential CHF risk factors were assessed at periodic clinic examinations. Outcome Measure. - The development of CHF. Results. - A total of 5143 eligible subjects contributed 72422 person-years of observation. During up to 20.1 years of follow-up (mean, 14.1 years), there were 392 new cases of heart failure; in 91% (357/392), hypertension antedated the development of heart failure. Adjusting for age and heart failure risk factors in proportional hazards regression models, the hazard for developing heart failure in hypertensive compared with normotensive subjects was about 2-fold in men and 3-fold in women. Multivariable analyses revealed that hypertension had a high population-attributable risk for CHF, accounting for 39% of cases in men and 59% in women. Among hypertensive subjects, myocardial infarction, diabetes, left ventricular hypertrophy, and valvular heart disease were predictive of increased risk for CHF in both sexes. Survival following the onset of hypertensive CHF was bleak; only 24% of men and 31% of women survived 5 years. Conclusions. - Hypertension was the most common risk factor for CHF, and it contributed a large proportion of heart failure cases in this population-based sample. Preventive strategies directed toward earlier and more aggressive blood pressure control are likely to offer the greatest promise for reducing the incidence of CHF and its associated mortality.

People who have the apolipoprotein (apo) E4 allele may have an increased risk of coronary heart disease (CHD). Apo E is a blood protein that can take different forms as determined by genetics. Alleles are alternative forms of a gene. Researchers examined and took blood samples from 1034 men and 916 women to evaluate the association between apo E alleles, abnormal blood fat levels, and CHD. Female patients with the apo E4 allele were more likely than male patients with the allele to have high total cholesterol levels and high low density lipoprotein levels than patients with the apo E2 allele. Both the E2 and E4 alleles were associated with moderately elevated triglyceride levels in men. Excessively high triglyceride levels were rare and occurred most often in men with the E2 allele. Fewer women over age 60 had the E4 allele compared to their younger counterparts. The E4 allele was associated with an increased risk of CHD in both men and women independent of CHD risk factors and blood lipid levels., Objective. - To describe the association between apolipoprotein E alleles ([epsilon]2, [epsilon]3, and [epsilon]4), dyslipidemias, and coronary heart disease (CHD). Design. - Cross-sectional prevalence study. Setting and Participants. - Community-based sample of men (n=1034) and women (n=916) aged 40 to 77 years who are participating in a long-term study of cardiovascular disease. Study participants underwent fasting lipid measurements, coronary risk factor determinations, and a comprehensive evaluation for the presence of current or previous CHD. Results. - Compared with the [epsilon]3 allele, the [epsilon]4 allele was associated with elevated low-density lipoprotein cholesterol values ([greater than or equal to]4.14 mmol/L [160 mg/dL]) in women, the [epsilon]2 and [epsilon]4 alleles were associated with moderately elevated triglyceride values ([greater than or equal to]2.82 mmo/L [250 mg/dL]) in men, and the [epsilon]2 allele was associated with severely elevated triglyceride values ([greater than or equal to]5.64 mmo/L [500 mg/dL]) in men. The apolipoprotein E alleles were not associated with hypertension, obesity, smoking, or diabetes, but the [epsilon]4 allele frequency was reduced in women after 60 years of age. The age-adjusted prevalence of CHD was associated when the [epsilon]4 allele in both men (relative odds=1.53, P=.04) and women (relative odds=1.99, P=.05). In analyses for women and for both sexes combined, this relation persisted after adjustment by hypertension, smoking, obesity, diabetes, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Conclusions. - Apolipoprotein E alleles are important genetic markers for dyslipidemia and CHD. The estimated CHD odds associated with the [epsilon]4 allele appears to be greater than that for any other known genetic lipid abnormality, and the association of the [epsilon]4 allele with CHD remains significant in women and both sexes combined after adjustment by traditional coronary desk factors and lipids.

Those with a disproportionately enlarged left heart ventricle appear to have a greater risk of stroke than those with normal-sized left ventricles. The relation of left ventricular mass (LVM) to body height was determined for 1,230 men and women aged 59 to 90 who were followed for eight years. The subjects suffered a total of 62 strokes and 27 transient ischemic attacks. The rate of stroke in the 25% of men with the highest LVM-to-height ratio was 18.4%. The corresponding rate for women was 12.2%. The rate for the 25% of men with the lowest LVM-to-height ratio was 5.2%, while women with the lowest LVM-to-height ratios had a rate of 2.9%. The overall increase in risk for the 25% with the highest LVM-to-height ratios compared to the 25% with the lowest LVM-to-height ratios was 2.72 after adjusting for factors such as age, blood pressure, smoking and diabetes. Enlarged LVM should be considered a risk factor for stroke., Objective.--To evaluate the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack in an elderly cohort. Design.--Cohort study with a follow-up period of 8 years. Setting.--Population-based sample. Subjects.--Elderly original cohort subjects of the Framingham Heart Study who were free of cerebrovascular disease and atrial fibrillation at the 16th biennial examination and who had adequate echocardiograms. This group consisted of 447 men (mean age, 67.8 years; range, 60 to 90 years) and 783 women (mean age, 69.2 years; range 59 to 90 years). Main Outcome Measures.--Age-adjusted 8-year incidence of stroke was examined as a function of baseline quartiles of LVM-to-height ratio. Proportional hazards regression was used in multivariate analyses to assess risk of stroke as a function of LVM-to-height ratio quartile, adjusting for age, sex, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, and blood lipid levels. Results.--Among the 1230 subjects eligible, 89 cerebrovascular disease events (62 strokes and 27 transient ischemic attacks) occurred during follow-up. In men, 8-year age-adjusted incidence of cerebrovascular events was 18.4% in the highest quartile of LVM-to-height ratio and 5.2% in the lowest quartile. Corresponding values in women were 12.2% and 2.9%. The hazard ratio for cerebrovascular events comparing highest to lowest quartile of LVM-to-height ratio was 2.72 (95% confidence interval [CI], 1.39 to 5.36) after adjusting for age, sex, systolic blood pressure, hypertension treatment, diabetes, cigarette smoking, and the ratio of total cholesterol to high-density lipoprotein cholesterol. After adjusting for age, sex, and cardiovascular disease risk factors, the hazard ratio for cerebrovascular events was 1.45 (95% CI, 1.17 to 1.80) for each quartile increment of LVM-to-height ratio. Conclusions.--Echocardiographically determined LVM-to-height ratio offers prognostic information beyond that provided by traditional cerebrovascular disease risk factors. Echocardiography provides information that facilitates identification of individuals at high risk for stroke and transient ischemic attack. (JAMA. 1994;272:33-36)

Continuous passive motion (CPM) may be more effective and less expensive than traditional physical therapy for rehabilitation of patients who have undergone total knee arthroplasty, or knee replacement surgery. This method involves the use of a CPM machine set for a certain rate and arc of motion to exercise the patient's knee. Among 93 patients with arthritis who underwent total knee arthroplasty, 48 were treated with CPM plus conventional physical therapy and 45 were treated with conventional physical therapy alone. Patients in the CPM group had increased active range of motion, less swelling and less need for manipulations, compared with those in the conventional physical therapy group. Patients treated with CPM did not experience significantly less pain or fewer complications than those who were not treated with CPM. Costs associated with treatment were less for patients in the CPM group than for those in the conventional physical therapy group., Objective.--To evaluate the efficacy of continuous passive motion (CPM) in the postoperative management of patients undergoing total knee arthroplasty. Design.--A randomized controlled single-blind trial of CPM plus standardized rehabilitation vs standard rehabilitation alone. Setting.--A referral hospital for arthritis and musculoskeletal care. Patients.--Consecutive patients with end-stage osteoarthritis or rheumatoid arthritis undergoing primary total knee arthroplasty who had at least 90[degree] of passive knee f exion. One hundred fifty-four patients were eligible and 102 patients agreed to participate and were randomized. Ninety-three patients completed the study protocol. Intervention.--Continuous passive motion machines programmed for rate and specified arc of motion within 24 hours of surgery with range increased daily as tolerated with standardized rehabilitation program compared with standardized rehabilitation program alone. Main Outcome Measures.--Primary outcomes were pain, active and passive knee range of motion, swelling (or circumference), quadriceps strength at postoperative day 7, as well as complications, length of stay, and active and passive range of mot on and function at 6 weeks. Results.--Use of CPM increased active flexion and decreased swelling and the need for manipulations but did not significantly affect pain, active and passive extens on, quadriceps strength or length of hospital stay. At 6 weeks there were no differences between the two groups in either range of motion or function. In this series, use of CPM resulted in a net savings of $6764 over conventional rehabilitation in achieving these results. Conclusion.--For the average patient undergoing total knee arthroplasty, CPM is more effective in improving range of motion, decreasing swelling, and reducing the need for manipulation than is conventional therapy and lowers cost. (JAMA. 1992;268:1423-1428)

The article presents information on vascular stiffness that increases as the age of the person increases and is the major cause of the age related morbidity and mortality. It informs that the stiffening of the aortic wall is associated with elevated pulse wave velocity (PWV) and prematurewave reflection that results in the increase in the pulsatile hemodynamic load, cardiac after load and reduces diastolic coronary flowing high flow organs such as the kidneys and brain. It further informs that the European Society of Cardiology considers elevated PWV a negative prognostic factor to be considered in the management of patients with hypertension

Importance: Aortic stenosis (AS) has no approved medical treatment. Identifying etiological pathways for AS could identify pharmacological targets., Objective: To identify novel genetic loci and pathways associated with AS., Design, Setting, and Participants: This genome-wide association study used a case-control design to evaluate 44 703 participants (3469 cases of AS) of self-reported European ancestry from the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort (from January 1, 1996, to December 31, 2015). Replication was performed in 7 other cohorts totaling 256 926 participants (5926 cases of AS), with additional analyses performed in 6942 participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Follow-up biomarker analyses with aortic valve calcium (AVC) were also performed. Data were analyzed from May 1, 2017, to December 5, 2019., Exposures: Genetic variants (615 643 variants) and polyunsaturated fatty acids (ω-6 and ω-3) measured in blood samples., Main Outcomes and Measures: Aortic stenosis and aortic valve replacement defined by electronic health records, surgical records, or echocardiography and the presence of AVC measured by computed tomography., Results: The mean (SD) age of the 44 703 GERA participants was 69.7 (8.4) years, and 22 019 (49.3%) were men. The rs174547 variant at the FADS1/2 locus was associated with AS (odds ratio [OR] per C allele, 0.88; 95% CI, 0.83-0.93; P = 3.0 × 10-6), with genome-wide significance after meta-analysis with 7 replication cohorts totaling 312 118 individuals (9395 cases of AS) (OR, 0.91; 95% CI, 0.88-0.94; P = 2.5 × 10-8). A consistent association with AVC was also observed (OR, 0.91; 95% CI, 0.83-0.99; P = .03). A higher ratio of arachidonic acid to linoleic acid was associated with AVC (OR per SD of the natural logarithm, 1.19; 95% CI, 1.09-1.30; P = 6.6 × 10-5). In mendelian randomization, increased FADS1 liver expression and arachidonic acid were associated with AS (OR per unit of normalized expression, 1.31 [95% CI, 1.17-1.48; P = 7.4 × 10-6]; OR per 5-percentage point increase in arachidonic acid for AVC, 1.23 [95% CI, 1.01-1.49; P = .04]; OR per 5-percentage point increase in arachidonic acid for AS, 1.08 [95% CI, 1.04-1.13; P = 4.1 × 10-4])., Conclusions and Relevance: Variation at the FADS1/2 locus was associated with AS and AVC. Findings from biomarker measurements and mendelian randomization appear to link ω-6 fatty acid biosynthesis to AS, which may represent a therapeutic target.

Importance: Nearly half of all patients with heart failure have preserved ejection fraction (HFpEF) as opposed to reduced ejection fraction (HFrEF), yet associations of biomarkers with future heart failure subtype are incompletely understood., Objective: To evaluate the associations of 12 cardiovascular biomarkers with incident HFpEF vs HFrEF among adults from the general population., Design, Setting, and Participants: This study included 4 longitudinal community-based cohorts: the Cardiovascular Health Study (1989-1990; 1992-1993 for supplemental African-American cohort), the Framingham Heart Study (1995-1998), the Multi-Ethnic Study of Atherosclerosis (2000-2002), and the Prevention of Renal and Vascular End-stage Disease study (1997-1998). Each cohort had prospective ascertainment of incident HFpEF and HFrEF. Data analysis was performed from June 25, 2015, to November 9, 2017., Exposures: The following biomarkers were examined: N-terminal pro B-type natriuretic peptide or brain natriuretic peptide, high-sensitivity troponin T or I, C-reactive protein (CRP), urinary albumin to creatinine ratio (UACR), renin to aldosterone ratio, D-dimer, fibrinogen, soluble suppressor of tumorigenicity, galectin-3, cystatin C, plasminogen activator inhibitor 1, and interleukin 6., Main Outcomes and Measures: Development of incident HFpEF and incident HFrEF., Results: Among the 22 756 participants in these 4 cohorts (12 087 women and 10 669 men; mean [SD] age, 60 [13] years) in the study, during a median follow-up of 12 years, 633 participants developed incident HFpEF, and 841 developed HFrEF. In models adjusted for clinical risk factors of heart failure, 2 biomarkers were significantly associated with incident HFpEF: UACR (hazard ratio [HR], 1.33; 95% CI, 1.20-1.48; P < .001) and natriuretic peptides (HR, 1.27; 95% CI, 1.16-1.40; P < .001), with suggestive associations for high-sensitivity troponin (HR, 1.11; 95% CI, 1.03-1.19; P = .008), plasminogen activator inhibitor 1 (HR, 1.22; 95% CI, 1.03-1.45; P = .02), and fibrinogen (HR, 1.12; 95% CI, 1.03-1.22; P = .01). By contrast, 6 biomarkers were associated with incident HFrEF: natriuretic peptides (HR, 1.54; 95% CI, 1.41-1.68; P < .001), UACR (HR, 1.21; 95% CI, 1.11-1.32; P < .001), high-sensitivity troponin (HR, 1.37; 95% CI, 1.29-1.46; P < .001), cystatin C (HR, 1.19; 95% CI, 1.11-1.27; P < .001), D-dimer (HR, 1.22; 95% CI, 1.11-1.35; P < .001), and CRP (HR, 1.19; 95% CI, 1.11-1.28; P < .001). When directly compared, natriuretic peptides, high-sensitivity troponin, and CRP were more strongly associated with HFrEF compared with HFpEF., Conclusions and Relevance: Biomarkers of renal dysfunction, endothelial dysfunction, and inflammation were associated with incident HFrEF. By contrast, only natriuretic peptides and UACR were associated with HFpEF. These findings highlight the need for future studies focused on identifying novel biomarkers of the risk of HFpEF.