Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MYOCARDIAL DISEASES, PRIMARY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources
PubMed1991

Cardiomyopathy: a necessary revision of the WHO classification.

The classification of myocardial disease proposed by the WHO/ISFC task force in 1980 distinguishes specific heart muscle diseases from myocardial diseases of unknown origin, termed cardiomyopathies, and differentiated into the dilated, hypertrophic and restrictive forms. This last group includes endomyocardiofibrosis and fibroblastic parietal endocarditis. In more recent years, two new forms of heart muscle disease have been recognized: so-called "primary" restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Primary restrictive cardiomyopathy is characterized anatomically by normally sized, non-hypertrophic ventricles with dilated atria, and functionally by impaired diastolic compliance due to myocardial stiffness. The clinical picture is that of chronic congestive heart failure; histology shows interstitial fibrosis and myocardial disarray, but not hypereosinophilia. In arrhythmogenic right ventricular cardiomyopathy, the myocardium of the right ventricular free wall is substituted by fibrous and/or adipose tissue, which results in regional dynamic alterations and ominous ventricular arrhythmias. The left ventricle is usually spared. Both forms should be classified as heart muscle diseases of unknown origin, and kept clearly distinct from the other cardiomyopathies listed in the WHO classification.

Arrhythmias, Cardiac↗
PubMed2000

[Is Na+Ca(2+) exchanger expression altered in the endomyocardium of patients with chronic heart valve diseases parallel to myocardial dysfunction?].

BACKGROUND: Na(+)-Ca2+ exchanger (EXCH) is an important regulator of intracellular calcium homeostasis. To maintain a normal intracellular Ca2+ concentration, EXCH expression may be upregulated before the onset of end-stage heart failure. We tested for a correlation between the EXCH transcription level and the degree of myocardial dysfunction as well as the suitability of EXCH transcription as a molecular marker for early detection of a transition from adequate to inadequate myocardial adaptation to chronic pressure and/or volume overload in valvular heart disease (VHD). METHODS: The level of EXCH transcription was analyzed in myocardial biopsies from eleven patients with aortic stenosis (AS), five with aortic regurgitation (AR) and six with primary mitral regurgitation (MR) of different hemodynamic severity and myocardial impairment using the quantitative rt-PCR technique. In addition, endomyocardial tissue from thirteen explanted hearts with end-stage heart failure and biopsies from seven individuals without heart disease were investigated. RESULTS: The mean level of EXCH transcription in patients with AS was: 1.8 +/- 1.4 amol/ng total RNA, with AR: 1.9 +/- 0.8 amol/ng and with MR: 2.2 +/- +2.1 amol/ng. This was not from different controls (2.6 +/- 1.2 amol/ng total RNA). However, in myocardium from end-stage heart failure, EXCH transcription was increased fourfold amounting to 8.9 +/- 1.9 amol/ng total RNA. No difference in the EXCH transcription was found in VHD with respect to the degree of myocardial dysfunction: cardiac index (CI) > 3.5 l/min/m2 (EXCH 1.4 +/- 1.1 amol/ng total RNA); CI 3.5-2.4 (EXCH 2.5 +/- 1.8); CI < 2.4 (EXCH 1.8 +/- 1.0); EF-angio > 50% (EXCH 1.9 +/- 1.8); EF-angio < or = 50% (EXCH 1.9 +/- 0.9); EF-RNV > 50% (EXCH 2.4 +/- 1.8), EF-RNV < or = 50% (EXCH 1.7 +/- 1.0). CONCLUSION: Myocardial EXCH transcription does not change parallel to the degree of myocardial dysfunction in VHD. Consequently, myocardial EXCH transcription does not appear to be suitable as a parameter indicating the transition from adequate to inadequate myocardial adaptation to chronic volume and/or pressure overload.

Adaptation, Physiological↗
PubMed1986

Myocardial diseases of animals.

In this review we have attempted a comprehensive compilation of the cardiac morphologic changes that occur in spontaneous and experimental myocardial diseases of animals. Our coverage addresses diseases of mammals and birds and includes these diseases found in both domesticated and wild animals. A similar review of the myocardial diseases in this broad range of animal species has not been attempted previously. We have summarized and illustrated the gross, microscopic, and ultrastructural alterations for these myocardial diseases; and, whenever possible, we have reviewed their biochemical pathogenesis. We have arranged the myocardial diseases for presentation and discussion according to an etiologic classification with seven categories. These include a group of idiopathic or primary cardiomyopathies recognized in man (hypertrophic, dilated, and restrictive types) and a large group of secondary cardiomyopathies with known causes, such as inherited tendency; nutritional deficiency; toxicity; physical injury and shock; endocrine disorders, and myocarditides of viral, bacterial, and protozoal causation. Considerable overlap exists between each of the etiologic groups in the spectrum of pathologic alterations seen in the myocardium. These include various degenerative changes, myocyte necrosis, and inflammatory lesions. However, some diseases show rather characteristic myocardial alterations such as vacuolar degeneration in anthracycline cardiotoxicity, myofibrillar lysis in furazolidone cardiotoxicity, calcification in calcinosis of mice, glycogen accumulation in the glycogenoses, lipofuscinosis in cattle, fatty degeneration in erucic acid cardiotoxicity, myofiber disarray in hypertrophic cardiomyopathy, and lymphocytic inflammation with inclusion bodies in canine parvoviral myocarditis. The myocardial diseases represent the largest group in the spectrum of spontaneous cardiac diseases of animals. Pericardial and endocardial diseases and congential cardiac diseases are seen less frequently; and, in contrast to man, coronary artery disease and myocardial ischemia are rather infrequent in animals. The present review shows clearly that the spectrum of myocardial diseases in animals is enlarging and that many newly recognized diseases are emerging and assuming considerable importance. For example, various heritable cardiomyopathies have recently been described in the KK mouse, cattle, and rats. Increasingly recognized myocardial diseases include cardiomyopathies in cats, dogs, and birds; anthracycline cardiotoxicity; furazolidone cardiotoxicity; ionophore cardiotoxicity; myocardial damage associated with central nervous system injuries; myocardial hypertrophy in

Animals↗
PubMed1992

Clinical characteristics of patients in studies of left ventricular dysfunction (SOLVD).

The Studies of Left Ventricular Dysfunction (SOLVD) trials were designed to evaluate the effects of enalapril on long-term mortality in patients with severe left ventricular (LV) dysfunction. Patients with LV ejection fractions less than or equal to 0.35 and symptoms of congestive heart failure (CHF) were enrolled in the treatment trial, whereas those with no history of overt CHF and taking no treatment directed for LV dysfunction were enrolled in the prevention trial. The baseline clinical characteristics of SOLVD patients were compared to characterize differences between patients in these 2 separate but concurrent trials. From over 70,000 patients screened with LV dysfunction, 4,228 patients were enrolled in the prevention trial and 2,569 patients in the treatment trial. Ischemic heart disease was the primary cause of LV dysfunction in both prevention (83%) and treatment (71%) trial patients. Prior myocardial infarction was present in 80% of the prevention and 66% of the treatment trial patients (p less than 0.001). In the prevention trial, infarction was recent (less than or equal to 6 months) in 27% patients and remote (greater than 6 months) in 57% patients. Treatment trial patients had proportionately more women (20 vs 13%; p less than 0.001) and non-Caucasians (20 vs 14%; p less than 0.001), as well as the coexisting risk factors of hypertension (42 vs 37%; p less than 0.001) and diabetes (26 vs 15%; p less than 0.001) than did prevention trial patients. Clinical characteristics of patients in both trials were influenced by the gender and race of enrolled patients. Similarly, coronary artery bypass surgery was performed less often in women and non-Caucasians.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1998

Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group.

CONTEXT: Observational studies have found lower rates of coronary heart disease (CHD) in postmenopausal women who take estrogen than in women who do not, but this potential benefit has not been confirmed in clinical trials. OBJECTIVE: To determine if estrogen plus progestin therapy alters the risk for CHD events in postmenopausal women with established coronary disease. DESIGN: Randomized, blinded, placebo-controlled secondary prevention trial. SETTING: Outpatient and community settings at 20 US clinical centers. PARTICIPANTS: A total of 2763 women with coronary disease, younger than 80 years, and postmenopausal with an intact uterus. Mean age was 66.7 years. INTERVENTION: Either 0.625 mg of conjugated equine estrogens plus 2.5 mg of medroxyprogesterone acetate in 1 tablet daily (n = 1380) or a placebo of identical appearance (n = 1383). Follow-up averaged 4.1 years; 82% of those assigned to hormone treatment were taking it at the end of 1 year, and 75% at the end of 3 years. MAIN OUTCOME MEASURES: The primary outcome was the occurrence of nonfatal myocardial infarction (MI) or CHD death. Secondary cardiovascular outcomes included coronary revascularization, unstable angina, congestive heart failure, resuscitated cardiac arrest, stroke or transient ischemic attack, and peripheral arterial disease. All-cause mortality was also considered. RESULTS: Overall, there were no significant differences between groups in the primary outcome or in any of the secondary cardiovascular outcomes: 172 women in the hormone group and 176 women in the placebo group had MI or CHD death (relative hazard [RH], 0.99; 95% confidence interval [CI], 0.80-1.22). The lack of an overall effect occurred despite a net 11% lower low-density lipoprotein cholesterol level and 10% higher high-density lipoprotein cholesterol level in the hormone group compared with the placebo group (each P<.001). Within the overall null effect, there was a statistically significant time trend, with more CHD events in the hormone group than in the placebo group in year 1 and fewer in years 4 and 5. More women in the hormone group than in the placebo group experienced venous thromboembolic events (34 vs 12; RH, 2.89; 95% CI, 1.50-5.58) and gallbladder disease (84 vs 62; RH, 1.38; 95% CI, 1.00-1.92). There were no significant differences in several other end points for which power was limited, including fracture, cancer, and total mortality (131 vs 123 deaths; RH, 1.08; 95% CI, 0.84-1.38). CONCLUSIONS: During an average follow-up of 4.1 years, treatment with oral conjugated equine estrogen plus medroxyprogesterone acetate did not reduce the overall rate of CHD events in postmenopausal women with established coronary disease. The treatment did increase the rate of thromboembolic events and gallbladder disease. Based on the finding of no overall cardiovascular benefit and a pattern of early increase in risk of CHD events, we do not recommend starting this treatment for the purpose of secondary prevention of CHD. However, given the favorable pattern of CHD events after several years of therapy, it could be appropriate for women already receiving this treatment to continue.

Aged↗
PubMedDate not supplied

History of treatment for depression: risk factor for myocardial infarction in hypertensive patients.

OBJECTIVE: Psychological factors have been suspected of contributing to the development of cardiovascular disease. This study examined the relationship between a self-reported history of treatment for depression and subsequent myocardial infarction among treated hypertensive patients. METHODS: Participants (5564) in a union-sponsored, hypertension control program in New York City, who entered the program during 1981-1994 without a history of cardiovascular disease and who were asked whether they had been treated for depression, were followed in a prospective cohort study. The primary outcome of interest was hospitalization or death due to myocardial infarction. RESULTS: At entry, 3.5% of men and 6.4% of women reported a history of treatment for depression. During 4.9 years (average) of follow-up, 112 fatal and nonfatal myocardial infarctions were recorded. The sex-adjusted relative risk of myocardial infarction was 2.24 (confidence interval = 1.13-4.45). Controlling for known cardiovascular risk factors with multivariate proportional hazards models, history of treatment for depression was significantly associated with subsequent myocardial infarction (hazard ratio = 2.10, confidence interval = 1.04-4.23). CONCLUSIONS: A self-reported history of treatment for depression is independently associated with subsequent myocardial infarction in treated hypertensive patients without prior cardiovascular disease. Whether additional or different treatment for depression will be cardioprotective is unknown and merits further study.

Adult↗
PubMed2000

[Genetic risk factors for myocardial infarct].

Interactions of genetic and environmental risk factors influence the susceptibility to coronary artery disease (CAD) and myocardial infarction. In myocardial infarction occurring at young age, genetics of this multifactorial disease may be the leading factor. A number of candidate genes have been implicated in the pathogenesis of CAD and myocardial infarction. Mutations in the DNA sequence (gene polymorphisms) have been identified that appear to play a crucial role in blood pressure regulation, lipid metabolism, endothelial function, in the pathophysiology of coagulation or thrombosis, or in interventional cardiology by interfering with restenosis development. Genetic polymorphisms seem to be clinically important because they not only potentiate the individual risk under certain circumstances, but they also determine safety and effectiveness of commonly prescribed drugs. Understanding the complexity and functional relevance of genetic risk factors will be useful in early detection and treatment of individuals that are exposed to higher risk for myocardial infarction. Thus it is important to include genetic risk factors in the concept of the classical risk factor theory. Potentially in future a genetic risk profile including relevant polymorphisms may be an essential part of the clinicians' knowledge in primary and secondary prevention of coronary artery disease.

Coronary Disease↗
PubMed1985

Psychological interventions in cardiovascular disease.

The literature on the behavioural treatment of primary hypertension, reduction of Type A behaviour, and psychological interventions during acute coronary care and rehabilitation after a myocardial infarction are selectively reviewed. There is growing evidence that relaxation and stress management can lower blood pressure by useful amounts in mild primary hypertension although the mechanisms underlying these reductions are unclear. Type A behaviour has been reduced in patients following a myocardial infarction and this led to reduced morbidity. Other interventions following myocardial infarction, both when the patient is in hospital and after discharge have produced at best only modest benefits and are, therefore, not widely applicable. Future research in rehabilitation should be directed at reducing the disabilities of patients with clearly identifiable problems that stem from their response to cardiovascular disease.

Adult↗
PubMed1975

Cardiac manifestations of Fabry's disease. Report of a case with mitral insufficiency and electrocardiographic evidence of myocardial infarction.

The light and electron microscopic findings in the heart of a patient with Fabry's disease are described. The study revealed that all cardiac tissues, including the conducting tissues and the valves, were involved. The latter finding was of particular interest since the patient was known to have mitral insufficiency. The findings of diffuse ballooning of the mitral valve with localized "overshoot" and massive glycolipid storage in the valve substance suggest that the abnormal storage process was itself responsible for the valvular insufficiency. The widespread involvement of the myocardium and conducting tissues is consistent with the elelctrocardiographic changes indicating infarction, although myocardial necrosis was not observed. The findings in this case suggest that the cardiac manifestations in Fabry's disease can be either primary, that is, directly related to the enzyme deficiency, or secondary, that is, evolving with time as a consequence of the disease.

Fabry Disease↗
PubMed1993

Plasma renin activity and ischemic heart disease.

BACKGROUND: An earlier prospective study reported an association between high levels of plasma renin activity (as measured by the renin-sodium profile) and the incidence of myocardial infarction in patients with hypertension. We have investigated the relation between plasma renin activity and ischemic heart disease in the Northwick Park Heart Study. METHODS: The study included 803 white men 40 to 64 years of age selected from industrial workers in London. Plasma renin activity and established risk factors for ischemic heart disease were measured at entry, which was between 1972 and 1978. Ascertainment of the primary clinical end points of fatal or nonfatal myocardial infarction and sudden death from coronary causes was carried out until the end of 1991. RESULTS: In an analysis of the 86 first coronary events, we found an independent relation between higher systolic blood pressure and coronary end points (relative risk per 1 SD increase in blood pressure, 1.47; 95 percent confidence interval, 1.16 to 1.85; P < 0.001), but no relation between plasma renin activity and coronary end points (relative risk per 1 SD increase in the level of plasma renin activity, 1.04; 95 percent confidence interval, 0.84 to 1.30). In the 242 men who had hypertension of a degree similar to that of the subjects in the earlier prospective study of the renin profile, and in whom 44 of the 86 coronary events occurred, the relative risk of those in the highest as compared with the lowest third for plasma renin activity was 1.26 (95 percent confidence interval, 0.63 to 2.56). CONCLUSIONS: Our results suggest that there is no association between plasma renin activity and myocardial infarction or sudden death from coronary causes, at least in normotensive men.

Adult↗
PubMedDate not supplied

Control of blood lipids in the elderly.

In individuals 65 years of age and older cardiovascular disease is the leading cause of death around the world. Hypercholesterolemia is among the major risk factors for the development of cardiovascular disorders. Most of the scientifically based studies on preventive measures for cardiovascular conditions have been conducted in subjects younger then 65 years of age. In the last 10 years some clinical trials have included a considerable number of individuals older than 65 years of age providing a scientific basis for therapeutic and preventive intervention in the aged. In this article we summarize the main studies concerning lipids as risk factors for cardiovascular disease in the elderly and we present the indicated primary and secondary preventive measures for reducing cholesterol levels in the elderly leading to a reduction in total and cardiac mortality, and to lesser development of myocardial infarction and coronary artery disease.

Age Factors↗
PubMed1994

Episodes of care for chest pain: a preliminary report from MIRNET. Michigan Research Network.

BACKGROUND: Although intensively studied in hospital and emergency settings, chest pain has remained largely unstudied in primary care, where it is associated with considerable diagnostic uncertainty and high utilization of medical resources. METHODS: We employed an established primary care research network to prospectively collect detailed information on episodes of care for chest pain. Over a 12-month period, Michigan Research Network (MIRNET) clinicians prospectively collected demographic, clinical, and clinician decision-making information for all patients seen in their offices with the complaint of chest pain. RESULTS: Three hundred ninety-nine complete episodes were collected and used for analysis. Episodes were well distributed among urban, rural, academic, and private sites. The average episode length was 1.53 visits. Musculoskeletal chest pain accounted for 20.4% of all diagnoses, followed by reflux esophagitis (13.4%) and costochondritis (13.1%). Stable angina pectoris was the primary diagnosis in only 10.3% of episodes, unstable angina or possible myocardial infarction in 1.5%. Most of the ancillary services used were directed toward finding or excluding cardiac disease. CONCLUSION: A practice-based network can be used to study episodes of care. Resource use during episodes of chest pain in primary care are directed toward exclusion of cardiac disease, despite the surprisingly low frequency of cardiac diagnoses.

Adult↗
PubMed2005

Pattern of exercise-induced ST change is related to coronary flow reserve in patients with chest pain and normal coronary angiogram.

OBJECTIVE: To evaluate the usefulness of exercise treadmill test in determining the true microvasculature-induced ischemia, we compared the pattern of ST depression with coronary flow reserve (CFR) using transthoracic Doppler echocardiography (TTE) in patients with chest pain and normal coronary angiogram. DESIGN: Fifty-nine subjects (M/F=21:38, mean age 55+/-9 years) with chest pain and normal coronary angiogram underwent maximal symptom-limited exercise treadmill test (ETT). CFR was estimated with TTE and dipyridamole. Patients with a history of acute myocardial infarction, regional wall motion abnormalities, hypertrophic cardiomyopathy, ejection fraction less than 50%, or primary valvular heart disease were excluded from this study. RESULTS: No ST change was observed in 20 of 59 (34%) patients, up slope depression was observed in 20 (34%), flat depression in 13 (22%), and down slope depression in 6 (10%). Eleven of thirty nine (28%) exercise positive patients had decreased CFR <2.1. CFR was 3.1+/-0.6 in group with no ST change, 3.1+/-0.6 in group with up slope depression, 2.1+/-0.6 in group with flat depression (p<0.05 versus group with no change and group with upslope depression, respectively), and 2.0+/-0.4 in group with down slope depression (p<0.05 versus group with no change and group with up slope depression, respectively). Flat to down slope depression of ST change during ETT had sensitivity of 58% and specificity of 95% for predicting CFR <2.1. CONCLUSION: Flat and down slope depression of ST segment during ETT might increase the sensitivity and specificity to detect the true microvasculature-induced ischemia that is defined as CFR less than 2.1 in patients with chest pain and normal coronary angiogram.

Aged↗
PubMed1997

Review of recent clinical trials of lipid lowering in coronary artery disease.

Early trials with lipid-lowering therapy in patients with established coronary artery disease revealed favorable trends in cardiovascular events but did not yield significant reductions in total mortality. Recent clinical trials using hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor ("statin") therapy have shown significant decreases in total mortality, cardiovascular events, hospitalizations, and the need for revascularization procedures, with its usage (1) to lower low-density lipoprotein (LDL) cholesterol after myocardial infarction (secondary prevention); and (2) in high-risk patients without evidence for coronary artery disease (primary prevention). Secondary prevention benefits have been seen for both men and women, in the young and elderly, and among diabetic and nondiabetic patients. The beneficial effects of LDL-cholesterol reduction occur early and are additive to other risk-reduction therapies. Lipid-lowering therapy should be part of the comprehensive treatment of all patients with atherosclerotic vascular disease and patients at high risk.

Anticholesteremic Agents↗