PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MYOCARDIAL DISEASES, PRIMARY”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 379 records · Page 21Linked to original sources
PubMed1995

Mitochondrial DNA mutations in myocardial diseases.

Recent genetic studies have revealed that some patients with primary cardiomyopathy (CM) possess mutations in the mitochondrial (mt) DNA of the myocardium (mtCM). Somatically acquired mutations such as deletions in mtDNA are caused mainly by hydroxyl radical damage to mtDNA. Cumulative accumulation of these somatic mutations during the life of an individual causes a bioenergetic deficit leading to myocardial dysfunction and cell death. The base-sequencing of the entire mtDNA from 48 individuals revealed that germ-line point mutations accelerate oxygen free radical damage and deletions, leading to the generation of many hundreds of types of mtDNA minicircles. These accelerated somatic mutations are expressed as premature ageing of the patients with mtCM. The comprehensive analyses of the entire mtDNA, including the base-sequencing and deletions correlating to the oxygen free radical damage, have revealed clear relationships between the genotype and its phenotype, with regard to, for example, the severity of clinical symptoms and the survival time of the patients. Extensive generation of mtDNA minicircles caused by the hydroxyl radical implies a close relationship between somatic mtDNA mutation and the programmed cell-death machinery.

Adolescent↗
PubMed1999

Effects of hypercholesterolemia on myocardial ischemia-reperfusion injury in LDL receptor-deficient mice.

Hypercholesterolemia is a primary risk factor for atherosclerosis, coronary artery disease, and myocardial infarction. We subjected low density lipoprotein receptor-deficient (LDLr -/-) and control (wild-type) mice to 30 minutes of myocardial ischemia and 120 minutes of reperfusion. Myocardial infarction per area at risk (AAR) was noted under baseline conditions to be significantly (P<0.05) smaller in the LDLr -/- mice compared with wild-type mice (24.7+/-3. 2% and 38.8+/-4.3% of AAR, respectively). Subsequently, mice were fed a high-cholesterol diet (HCD) for 2 or 12 weeks, which resulted in significant increases in serum cholesterol levels in both LDLr -/- and wild-type groups. After 2 weeks of the HCD, the LDLr -/- mice demonstrated a significant elevation (P<0.01) in myocardial necrosis per AAR (50.2+/-5.36% of AAR) compared with the normal-diet LDLr -/- group, whereas the short-term HCD-fed wild-type mice demonstrated no significant difference from baseline. In contrast, wild-type mice fed the HCD for 12 weeks revealed a significant (P<0. 05) decrease in necrosis per AAR, which was 22.5+/-3.2% of the AAR in comparison with that in the normal-diet wild-type mice (38.8+/-4. 3% of AAR). LDLr -/- mice on the same long-term HCD showed a similar significantly (P<0.05) decreased infarct size, which was 13.2+/-4.0% of the AAR. In additional experiments, we determined that myocardial tissue total glutathione (GSH) levels were reduced after 2 weeks of the HCD and were significantly increased after 12 weeks of the HCD in the LDLr -/- mouse heart. These data suggest that short-term cholesterol feeding renders the myocardium of LDLr -/- mice more susceptible to ischemia-reperfusion injury, whereas more long-term hypercholesterolemia confers cardioprotection in the LDLr -/- mouse heart.

Animals↗
PubMed1997

Familial and primary (AL) cardiac amyloidosis: echocardiographically similar diseases with distinctly different clinical outcomes.

OBJECTIVE: To determine whether patients with myocardial amyloidosis due either to AL (primary) amyloid or familial amyloid have distinguishing echocardiographic or electrocardiographic features; and to compare the prevalence of heart failure and survival in the two types of amyloidosis in relation to echocardiographic findings. DESIGN: Blinded group comparison of randomly selected cases of cardiac amyloidosis. SETTING: International referral centre for amyloid research and treatment. PATIENTS: 36 patients with cardiac amyloid heart disease, of whom 12 had familial and 24 had primary AL amyloidosis. RESULTS: Familial and AL echocardiograms were morphologically indistinguishable, with similar left ventricular wall thickness, mean (SD) 15.4 (2.3) nu 15.8 (2.5) mm, respectively; right ventricular wall thickness was also similar between amyloid types: 9.6 (2.8) nu 9.7 (6.5) mm, respectively. Doppler indices of left and right ventricular function, left ventricular volume, and ejection fraction were also similar. Low voltage electrocardiograms (< 0.5 mV) were more common in the AL (16/24, 67%) than in the familial group (4/12, 25%), P < 0.05. The one year survival for familial and AL forms was 92% (11/12) nu 38% (6/24), respectively, with virtually all deaths due to cardiac causes. CONCLUSIONS: Although cardiac involvement is echocardiographically indistinguishable, cardiac mortality is very different between the two forms of amyloidosis. Preservation of electrocardiographic voltage in familial amyloidosis suggests that the particular biochemical characteristics of distinct types of amyloid fibril have different pathological effects on the myocardium. This distinction becomes critical in the evaluation, treatment, and management of patients who have a diagnosis within the spectrum of the protein deposition diseases.

Amyloidosis↗
PubMed1976

Hepato- and cardiotoxicity of xanthoascin, a new metabolite of A. candidus Link, to mice. I. Blood chemistry and histological changes in mice.

Aspergillus candidus Link, one of the commonest constituents of cereal mycoflora, produces two kinds of mycotoxins, terphenyllin and xanthoascin, which show different chemical and toxicological properties. The latter, xanthoascin, caused severe hepatic injury with jaundice and focal or confluent necrosis of hepatocytes, when given to mice in doses of 6 mg/kg b.w. or higher by a single subcutaneous injection. With higher doses above 15 mg/kg, myocardial degeneration and necrosis was induced after a week or two in addition to the hepatic injury. Vacuolation of the nuclei of the alveolar interstitial cells of the lung and myocardial interstitial cells was another characteristic lesion caused by this mycotoxin. Other organs including the testicles and thymus were widely involved. The unique nature of lesions in the liver and heart may necessitate further investigations in the field of mycotoxicology in relation to human diseases such as nutritional hepatitis and primary myocardial degeneration.

Administration, Oral↗
PubMed1985

Tuberculosis. Cause of death in antibiotic era.

A five-year review (1979 to 1983) of 41 patients with active tuberculosis at the time of death was performed to determine the cause of death. Twenty deaths (49 percent) were directly attributed to tuberculosis. Overwhelming tuberculous disease was the cause of death for seven patients, and among them the majority had strikingly low serum levels of albumin. Ten patients died of either massive hemoptysis or respiratory failure. Only two patients died due to progressive drug-resistant disease in an area where drug resistance is common. The majority of patients (21/41; 51 percent) died of common medical problems unrelated to tuberculosis. Eleven patients died from cardiopulmonary disease (five pulmonary emboli, one respiratory failure due to chronic obstructive pulmonary disease, two acute myocardial infarctions, and two primary dysrhythmias). Three deaths were the result of gastrointestinal bleeding, and three patients died as a result of bacterial superinfection. Our data indicate that patients still die of tuberculosis in the era of effective antituberculosis therapy. It is imperative that clinicians are aware that pulmonary emboli, arteriosclerotic heart disease, bacterial superinfection, and gastrointestinal bleeding cause approximately 50 percent of the deaths among patients who have tuberculosis and that prompt recognition and treatment of those diseases might decrease the mortality from tuberculosis.

Adolescent↗
PubMed2004

There is no evidence for an increase in acute coronary syndromes after short-term abrupt discontinuation of statins in stable cardiac patients.

BACKGROUND: For a variety of reasons, many patients abruptly discontinue statin therapy. The present analysis was conducted to determine whether the risk of cardiovascular outcomes increases after withdrawal of statin therapy in a stable cardiac population. METHODS AND RESULTS: In the Treating to New Target (TNT) study, 2 doses of atorvastatin (10 and 80 mg once daily) are being used in a double-blind parallel-group design. Of the 18,468 patients screened for study participation, 16,619 entered a dietary lead-in/drug-washout period, and of these, 15,432 eligible participants began treatment with atorvastatin 10 mg/d on an open-label basis. Of the subjects who entered the dietary lead-in/drug-washout period, 57% were receiving prior statin therapy. During the 6-week drug-washout period, there were 24 primary events (defined as coronary heart disease death, nonfatal myocardial infarction, resuscitated cardiac arrest, and fatal or nonfatal stroke); throughout the subsequent 8-week open-label period, there were 31 primary events. This equated to monthly Kaplan-Meier event rates of 0.20% during washout and 0.26% in the open-label phase. Event rates were therefore similar during the 2 phases. CONCLUSIONS: The present analysis demonstrates that short-term discontinuation of statin therapy in stable cardiac patients apparently does not lead to a clinically important increased risk of acute coronary syndromes.

Acute Disease↗
PubMed1997

Primary hyperparathyroidism with cardiac abnormalities: a case report.

Primary hyperparathyroidism, characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia, is quite common in the elderly. Most patients with primary hyperparathyroidism have only mild hypercalcemia and are symptomless. But others experience various other organ diseases. Primary hyperparathyroidism is also associated with cardiovascular abnormalities, including QT interval shortening, heart block, cardiac arrhythmias, hypertension, myocardial hypertrophy, myocardial calcification and, though rarely, with valvular heart disease. We described a case of primary hyperparathyroidism associated with cardiac abnormalities. An 82-year-old male presented with the complaints of chest discomfort, fatigue, general weakness, nausea and vomiting over a period of months and was admitted in July 1996. Physical examination with heart auscultation showed a pansystolic murmur over the right sternal border and apex region, and a blowing diastolic murmur over the left sternal border. Biochemistry profiles revealed elevations of serum calcium (14.3 mg/dl) and chloride/phosphate ratio (> 33). Endocrinological studies showed elevations of serum PTH-C (4.8 ng/ml) and PTH-intact (705 pg/ml) concentrations. Kidney ultrasonography revealed a left renal stone. A spine X-ray revealed spondylosis and a compression fracture of the lumbar-spine with osteoporotic change. Thyroid ultrasonography and Thallium (Tl201)-technetium (Tc99m) subtraction scan showed parathyroid adenoma in the low pole of the right thyroid bed. Parathyroid aspiration cytology revealed few and discrete cells. Echocardiogram revealed moderate to severe aortic valvular calcification as well as stenosis with moderate aortic regurgitation, mitral regurgitation and myocardial calcification. The patient received parathyroidectomy one month later. During his postoperative days, he suffered from muscle twitching with positive Trousseau's sign and Chvostek's sign. The patient received calcium carbonate and vitamin D for hypocalcemia, diltiazem and capoten for his heart problems. A repeated echocardiogram two months after surgery showed no improvement of valvular calcification.

Aged↗
PubMedDate not supplied

Primary diastolic heart failure.

Diastolic heart failure is defined clinically when signs and symptoms of heart failure are present in the presence of preserved left ventricular systolic function (ejection fraction >45%). The incidence and prevalence of primary diastolic heart failure increases with age and it may be as high as 50% in the elderly. Age, female gender, hypertension, coronary artery disease, diabetes, and increased body mass index are risk factors for diastolic heart failure. Hemodynamic consequences such as increased pulmonary venous pressure, post-capillary pulmonary hypertension, and secondary right heart failure as well as decreased cardiac output are similar to those of systolic left ventricular failure, although the nature of primary left ventricular dysfunction is different. Diagnosis of primary diastolic heart failure depends on the presence of preserved left ventricular ejection fraction. Assessment of diastolic dysfunction is preferable but not mandatory. It is to be noted that increased levels of B-type natriuretic peptide does not distinguish between diastolic and systolic heart failure. Echocardiographic studies are recommended to exclude hypertrophic cardiomyopathy, infiltrative heart disease, primary valvular heart disease, and constrictive pericarditis. Myocardial stress imaging is frequently required to exclude ischemic heart disease. The prognosis of diastolic heart failure is variable; it is related to age, severity of heart failure, and associated comorbid diseases such as coronary artery disease. The prognosis of severe diastolic heart failure is similar to that of systolic heart failure. However, cautious use of diuretics and/or nitrates may cause hypotension and low output state. Heart rate control is essential to improving ventricular filling. Pharmacologic agents such as angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers are used in selected patients to decrease left ventricular hypertrophy. To decrease myocardial fibrosis, aldosterone antagonists have a potential therapeutic role. However, prospective controlled studies will be required to establish their efficacy in primary diastolic heart failure.

Aged↗
PubMed2006

Abciximab in ST-elevation acute myocardial infarction occurring in a heart transplant recipient and treated with stenting.

The authors describe primary coronary intervention consisting of direct stenting after abciximab administration in a case of acute anterior myocardial infarction occurring in a heart transplant recipient with triple-vessel disease. Primary success was obtained and the patient survived to a one-year angiographic follow up which showed persistent coronary patency. This is the first report concerning the use of abciximab in primary stenting for acute myocardial infarction in allograft coronary artery disease.

Abciximab↗
PubMed2001

Aspirin in cardiovascular disease.

The historic genesis of aspirin as a therapeutic agent is discussed. The use of aspirin as a primary and secondary chemo-preventive agent is reviewed. Those who introduced aspirin in the late 19th century would be surprised by the uses of aspirin today. It is anticipated that existing and further studies on the use of aspirin as a primary preventive agent will establish its utility and a more precise niche for it as a chemo-preventive agent. Reports indicate that it may be useful as a chemo-preventive agent in the prevention and possibly in the treatment of cancer of the colon and other malignancies. This plebeian drug, aspirin, has earned a position, some would say an egalitarian position, along with thrombolysis and primary coronary angioplasty in the emergency treatment of AMI. There are those who would add an intravenous beta blocker and an ACE inhibitor to this regimen. The laborious history of aspirin should again remind clinicians that they should continue to heed the admonition of Alexander Pope when he asserted, "Be not the first by whom the new is tried nor yet the last to lay the old aside."

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Long-term low-molecular-weight heparin (Fragmin) and/or early revascularization during instability in coronary artery disease (the FRISC II Study).

The Fragmin and/or Early Revascularisation during Instability in Coronary Artery Disease (FRISC II) trial will, in a prospective multicenter factorially randomized study, compare the efficacy of 3 months continuation of subcutaneous treatment with the low-molecular-weight heparin dalteparin (Fragmin) with that of placebo and will also compare a direct invasive strategy with a stepwise selective approach with regard to the utilization of coronary angiography and revascularization in patients with unstable coronary artery disease. The primary endpoints are death or myocardial infarction after 3 and 6 months respectively. Secondary endpoints are the same events after 12-24 months and also cardiac symptoms, exercise capacity, and/or signs of myocardial ischemia, readmission, and costs. Analyses will also be made of subgroups based on inclusion diagnosis, initial elevation of biochemical markers of myocardial damage, elevation of fibrinogen or C-reactive protein, signs of ischemia in electrocardiography at rest or at continuous 24-hour ischemia monitoring, and left ventricular function at echocardiography. Altogether, 3,100 patients will be recruited in 65-70 Scandinavian centers. Completion of follow-up is anticipated in the second half of 1998. The FRISC II study will further elucidate new alternatives for antithrombotic, invasive, and individually tailored treatment of unstable coronary syndromes.

Angina, Unstable↗
PubMed1981

[Lipid analytic investigations concerning the establishment of the forms of primary hypercholesterolaemia in patients with myocardial infarction].

The influence of genetic factors in the development of the coronary heart disease can be particularly impressively clarified at the instance of the primary hyperlipoproteinaemias. The exact diagnostics of the genetically determined disturbances of lipometabolism in patients with infarction is, however, still connected with difficulties. Determinations of serum cholesterol and triglycerides, lipid-electrophoretic recognitions as well as determinations of LDL- and HDL-cholesterol in the serum cannot always outline with utmost clearness the proportion of primary hyperlipoproteinaemias in the morbidity of infarctions. Before this background the practical value of the radiochemical screening test worked up at the model of lymphocytes is emphasized, which allows a clear diagnosis of primary forms of hypercholesterolaemia according to pathogenetic viewpoints and thus renders possible also family examinations within the primary prevention of the coronary heart disease.

Adolescent↗
PubMed1985

[Detection of anterior interventricular involvement after primary posterior wall infarct].

Forty-five patients (average age 53.3 +/- 9.4 years) underwent exercise stress testing coupled with exercise myocardial scintigraphy and right heart catheterisation on exercise during the 3rd week after primary posterior wall infarction. Coronary angiography and ventriculography were carried out 24 to 48 hours later. Significant (greater than or equal to 75%) left anterior descending disease was present in 9 patients (Group I) and absent in 36 patients (Group II). Tolerance of maximal exercise stress testing was good in all patients. The results were uninterpretable in on third of the cases because the theoretical maximal heart rate was not attained. No significant difference was noted between groups I and II with respect to: mean age, percentage of theoretical maximal heart rate attained, mean pulmonary capillary pressures at rest and during exercise, basal and exercise cardiac index, end diastolic index and angiographic left ventricular ejection fraction. The sensitivity and specificity for the detection of LAD disease were 80% and 84% for the exercise stress testing (n = 30), 44% and 75% for exercise right heart catheterisation (n = 30), 60% and 92% for exercise myocardial scintigraphy (n = 30), 100% and 75% for combined exercise stress testing and myocardial scintigraphy (n = 30) and 78% and 64% for combined exercise stress testing and myocardial scintigraphy and exercise right heart catheterisation (n = 45). These results show that in patients capable of performing maximal exercise stress tests, the best method of early detection of significant LAD disease after primary posterior infarction was combined exercise stress testing and exercise myocardial scintigraphy. These investigations are useful for the selection of candidates for coronary angiography.

Adult↗
PubMed1977

Pathophysiology of myocardial infarction.

Primary prevention of death from ischemic heart disease requires further understanding of the pathogenesis of this disorder. Cellular defects of cholesterol metabolism may be more significant markers that serum lipid levels for the identification and treatment of atherosclerotic risk. Coronary spasm has been shown to be an important cause of ischemia in the presence and absence of atherosclerotic lesions. Careful manipulation of physiologic variables with vasodilator agents during cardiopulmonary bypass can substantially alter the myocardial oxygen supply-demand relation, thereby minimizing ischemic injury. The cellular basis for loss of mechanical function during ischemia and the factors that determine irreversible injury are yet unknown.

Action Potentials↗
PubMed1991

Unique cardioprotective potential of angiotensin converting enzyme inhibitors: a hypothesis still to be tested on humans.

'Primary cardioprotection' has, arguably, already been shown with thiazide diuretics and probably with beta-blockers. The proven safety and efficacy of these established drugs override any theoretical or experimental considerations in favour of ACE inhibitors. It is unfortunate that, as yet, the number of hypotheses generated in support of ACE inhibitors has not been matched by large scale clinical trials employing these drugs. The first report of the clinical use of an ACE inhibitor was in 1984; it is high time comparative studies with conventional, and proven, agents were undertaken. With regard to 'secondary cardioprotection', there is overwhelming evidence in favour of the use of beta-blockers in patients with myocardial ischaemia. Indeed, we would argue that ACE inhibitors should be used with caution in such patients to avoid impairment of coronary infusion. In the patient with acute myocardial infarction, intravenous nitrates are cheap, easy to use, safe and seem to be effective (in preventing early remodelling and reducing mortality). In the subacute phase, beta-blockers improve prognosis and, according to the currently available evidence in humans, nitrates are as effective as captopril in altering late remodelling; as in the acute situation, nitrates are cheaper, simpler to use and have a track record of long-term safety. ACE inhibitors improve symptoms, exercise capacity and prognosis in chronic heart failure. In this condition, they have been a major therapeutic advance and, on the available evidence, are to be initially preferred to other vasodilators though they should be given in addition to diuretics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1997

Regulation of contractile proteins in diabetic heart.

Diabetes is one of the most prevalent chronic conditions that has a high association with death from cardiovascular disease(s). An impaired cardiac function independent of vascular disease suggests the existence of a primary myocardial defect in diabetes mellitus. We and others have documented that myocardial performance is impaired in the hearts of chronically diabetic rats and rabbits. Abnormalities in the contractile proteins and regulatory proteins could be responsible for the mechanical defects in streptozotocin (STZ)-diabetic hearts. The major focus of research on contractile proteins in the diabetic state has been on myosin ATPase and its isoenzymes. However, in the contractile protein system, this could be only one of the mechanisms that might be a controlling factor in myofilament contraction in diabetes. To define the role of cardiac contractile as well as regulatory proteins (troponin-tropomyosin) as a whole in the regulation of actomyosin system in diabetic cardiomyopathy, individual proteins of the cardiac system were reconstituted under controlled conditions. Enzymatic data confirmed a diminished calcium sensitivity in the regulation of the cardiac actomyosin system when regulatory protein(s) complex was recombined from diabetic hearts. This diminished calcium sensitivity along with shifts in cardiac myosin heavy chain (V1-->V3) could contribute to the impaired cardiac function in the hearts of chronic diabetic rats. It has also been reported that sarcomeric proteins such as myosin light chain-2 (MLC-2) and troponin I (TnI) could be involved in regulating muscle contraction and in calcium sensitivity. Since phosphorylation of cardiac TnI is associated with altered maximum enzymatic activity and calcium force relationship in isolated muscle preparations. TnI phosphorylation could contribute to depressed myocardial contractility in experimental diabetes. While we have yet to understand the exact function of each component in cardiac muscle and their behavior in concert where all of them act in tandem, we have focussed on the role of contractile proteins and their regulation in diabetes in this review. We have also included a brief discussions on other relevant intracellular components. In summary, there is substantial evidence to suggest that there are independent processes associated with diabetes which effect cardiac performance in experimental animals and in man. The focus of this review has been the explication of a biochemical defect which underlies cardiac contractile dysfunction in experimental models of diabetes.

Animals↗