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At least 415 records · Page 23Linked to original sources
PubMed1998

Antiarrhythmic drugs and devices for the management of ventricular tachyarrhythmia in ischemic heart disease.

Ischemic heart disease is the most frequent cardiac abnormality in patients with sustained or nonsustained ventricular tachyarrhythmias. The goals of therapy in such patients are to decrease the severity and incidence of symptoms and prolong life. In this article, we review the current views on antiarrhythmic drug therapy and an implantable cardioverter-defibrillator (ICD) in patients with ischemic heart disease. The importance of beta blockade as part of the therapy is emphasized. In addition, the superiority of sotalol and amiodarone over class I drugs, the benefits of combined treatment with amiodarone and a beta blocker, and the impact and limitations of current trials comparing the effectiveness of drug therapy with that of an ICD are all considered. Also discussed is the combined use of an antiarrhythmic drug and an ICD. In this approach sotalol is generally the agent of choice, with amiodarone the second choice.

Anti-Arrhythmia Agents↗
PubMed2003

Sex differences in risk for coronary heart disease mortality associated with diabetes and established coronary heart disease.

BACKGROUND: The sex-specific independent effect of diabetes mellitus and established coronary heart disease (CHD) on subsequent CHD mortality is not known. METHODS: This is an analysis of pooled data (n = 5243) from the Framingham Heart Study and the Framingham Offspring Study with follow-up of 20 years. At baseline (1971-1975), 134 men and 95 women had diabetes, while 222 men and 129 women had CHD. Risk for CHD death was analyzed by proportional hazards models, adjusting for age, hypertension, serum cholesterol levels, smoking, and body mass index. The comparative effect of established CHD vs diabetes on the risk of CHD mortality was tested by testing the difference in log hazards. RESULTS: The adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) for death from CHD were 2.1 (95% CI, 1.3-3.3) in men with diabetes only, and 4.2 (95% CI, 3.2-5.6) in men with CHD only compared with men without diabetes or CHD. The HR for CHD death was 3.8 (95% CI, 2.2-6.6) in women with diabetes, and 1.9 (95% CI, 1.1-3.4) in women with CHD. The difference between the CHD and the diabetes log hazards was +0.73 (95% CI, 0.72-0.75) in men and -0.65 (95% CI, -0.68 to -0.63) in women. CONCLUSIONS: In men, established CHD signifies a higher risk for CHD mortality than diabetes. This is reversed in women, with diabetes being associated with greater risk for CHD mortality. Current treatment recommendations for women with diabetes may need to be more aggressive to match CHD mortality risk.

Adult↗
PubMed2003

New directions in strategies using cell therapy for heart disease.

Congestive heart failure remains a major public health problem and is frequently the end result of cardiomyocyte apoptosis and fibrous replacement after myocardial infarction, a process referred to as left ventricular remodeling. Cardiomyocytes undergo terminal differentiation soon after birth and are generally considered to irreversibly withdraw from the cell cycle. In response to ischemic insult adult cardiomyocytes undergo cellular hypertrophy, nuclear ploidy, and a high degree of apoptosis. A small number of human cardiomyocytes retain the capacity to proliferate and regenerate in response to ischemic injury. However, whether these cells are derived from a resident pool of cardiomyocyte stem cells or from a renewable source of circulating bone marrow-derived stem cells that home to the damaged myocardium is at present not known. Replacement and regeneration of functional cardiac muscle after an ischemic insult to the heart could be achieved by either stimulating proliferation of endogenous mature cardiomyocytes or resident cardiac stem cells or by implanting exogenous donor-derived or allogeneic cells such as fetal or embryonic cardiomyocyte precursors, bone marrow derived mesenchymal stem cells, or skeletal myoblasts. The newly formed cardiomyocytes must integrate precisely into the existing myocardial wall in order to augment synchronized contractility and avoid potentially life-threatening alterations in the electrical conduction of the heart. A major impediment to survival of the implanted cells is altered immunogenicity by prolonged ex vivo culture conditions. In addition, concurrent myocardial revascularization is required to ensure viability of the repaired region and prevent further scar tissue formation. Human adult bone marrow contains endothelial precursors which resemble embryonic angioblasts and can be used to induce infarct bed neovascularization after experimental myocardial infarction. This results in protection of cardiomyocytes against apoptosis, induction of cardiomyocyte proliferation and regeneration, long-term salvage and survival of viable myocardium, prevention of left ventricular remodeling, and sustained improvement in cardiac function. It is reasonable to anticipate that cell therapy strategies for ischemic heart disease will need to incorporate (a) a renewable source of proliferating, functional cardiomyocytes, and (b) angioblasts to generate a network of capillaries and larger size blood vessels for supply of oxygen and nutrients to both the chronically ischemic endogenous myocardium and to the newly implanted cardiomyocytes

Adult↗
PubMed1999

Seasonal variations in coronary heart disease.

Coronary heart disease exhibits a winter peak and summer trough in incidence and mortality, in countries both north and south of the equator. In England and Wales, the winter peak accounts for an additional 20,000 deaths per annum. It is likely that this reflects seasonal variations in risk factors. Seasonal variations have been demonstrated in a number of lifestyle risk factors such a physical activity and diet. However, a number of studies have also suggested a direct effect of environmental temperature on physiological and rheological factors. We review the available evidence on seasonal variations in coronary heart disease and possible explanations for them.

Cold Climate↗
PubMed1984

Genetic research in coronary heart disease.

Coronary heart disease research along genetic lines is difficult. Studies in molecular genetics of apolipoprotein and receptor variability appear most promising in the near future. However, unexpected discoveries and methodology may turn up that may completely change the field. Exclusive concentration on lipid research therefore should be avoided. It is likely that most advances will come from carefully designed studies that ask specific questions. Such research design is appropriate not only for laboratory studies but also for clinical and epidemiological investigations. The collaboration of clinicians, biochemists, geneticists, epidemiologists, and statisticians is likely to lead to better understanding of coronary heart disease.

Alleles↗
PubMed1999

Coronary heart disease is a multifactorial disease.

Coronary heart disease (CHD) is the leading cause of death in the Western World. For effective treatment and prevention strategies to be put in place, the major risk factors associated with this disease must be identified. Data show that almost 300 variables are statistically associated with CHD. However, evidence suggests that the vast majority of coronary events can be explained on the basis of blood pressure, lipids, smoking, and diabetes. Laboratory, experimental, and epidemiologic data identify dyslipidemia as a pivotal CHD risk factor, in the absence of which other risk factors cease to produce any important increase in absolute risk of events. For example, in populations with relatively low levels of low-density lipoprotein cholesterol, such as China and Japan, the incidence of CHD remains low even when smoking and hypertension are highly prevalent. Observational data have clearly established that CHD risk factors tend to cluster in individuals. The impact of coexisting risk factors is greater than additive, and indeed is usually multiplicative. The implications of such an interactive effect are that relatively normal levels of two or more risk factors in coexistence may have a profound impact on risk. Despite these findings, in the past most treatment algorithms have viewed risk factors separately and have recommended discrete treatment targets. More recent guidelines have taken a broader view and provide simple, yet accurate, methods of evaluating absolute risk based on the consideration of several risk factors. Coronary heart disease is clearly a multifactorial disease with risk factors that tend to cluster and interact in an individual to determine the level of coronary risk. The current trend towards a more holistic approach in CHD risk evaluation and preventive management appears logical based on evidence from animal-experimental, observational, and clinical trial evidence.

Animals↗
PubMed1992

Platelet aggregation and coronary heart disease risk factor variation in Australian populations with different coronary heart disease mortality.

In a cross-sectional analytic study, we examined the differences in coronary heart disease (CHD) risk factors, including coagulation factors and platelet aggregation, among males from southern European countries and those of Anglo-Celtic descent who had widely different CHD standardized mortality ratios. The participants included 169 men aged 40 to 49 years, 27% of whom were born in southern European countries. The subjects had no history of heart disease and no other clinical conditions, or were not taking medications known to affect hemostasis. Data obtained included their medical history and CHD-related risk behaviors, blood pressure, height, weight, abdominal and pelvic circumference, and coagulation, fibrinolysis, platelet activity, lipids, and lipoproteins profiles. There were significant differences between the two groups in the prevalence of a positive family history, mean apolipoprotein A1 levels, and platelet aggregation responses to ADP. Other established risk factors, including coagulation factor levels, were not significantly different.

Adenosine Diphosphate↗
PubMed2001

Heart rate variability in ischemic heart disease.

Major untoward events, such as life-threatening arrhythmias and acute coronary events, have been suggested to be triggered by the activation of the autonomic nervous system in patients with coronary artery disease. Analysis of heart rate variability by conventional time and frequency domain methods, as well as by newer methods derived from nonlinear system theory, has offered a novel approach for studying the abnormalities in cardiovascular neural regulation in ischemic heart disease. Heart rate variability has been shown to be altered among patients with ischemic heart disease as compared to their age-matched controls without the evidence of ischemic heart disease. There are also obvious differences in various measures of heart rate variability between patients with uncomplicated coronary artery disease and those with coronary artery disease with complicated myocardial infarction. Impaired high-frequency oscillations of heart rate is the most prominent feature in patients with uncomplicated coronary artery disease, suggesting mainly an impairment in vagal autonomic regulation. Patients with prior myocardial infarction have a reduced overall heart rate variability, and a specific spectral pattern with a reduced low-frequency spectral component has been observed in patients with prior myocardial infarction and impaired left ventricular function. Recent studies have shown that the new nonlinear measures, particularly fractal analysis methods of heart rate dynamics, can detect subtle changes in heart rate behavior that are not easily detected by traditional analysis methods from ambulatory recordings. Patients with prior myocardial infarction have steeper power-law slope analyzed from the ultra and very low-frequency spectral bands, and they also have more random short-term heart rate dynamics analyzed by the detrended fluctuation method. A large body of data indicate that reduced overall heart rate variability is associated with an increased risk of mortality and nonfatal cardiac events in patient with ischemic heart disease. Of particular note, recent studies indicate that fractal analysis methods perform even better than the traditional analysis methods of heart rate variability as predictors of death and the onset of life-threatening arrhythmic events in post-infarction populations. These findings support the notion that heart rate variability analysis methods, such as fractal and complexity measures as well as conventional techniques, give valuable clinical information among patients with ischemic heart disease.

Autonomic Nervous System↗