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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the leading causes of mortality in diabetics is myocardial disease. In the past few years this subject has generated a significant amount of interest with the result that myocardial problems associated with diabetes are far better understood. Though originally thought to occur as a result of atherosclerosis, various studies have shown that heart disease can occur in the absence of atherosclerosis, suggesting a diabetic cardiomyopathy. Using diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Diabetic rat hearts do not respond to conditions of high stress as well as controls. The functional depression is accompanied by altered cardiac enzyme systems. A decrease in myosin ATPase activity which appears to be a result of diabetes-induced hypothyroidism is seen. Also, a depression of sarcoplasmic reticular calcium ATPase, along with a depression of calcium uptake by the SR, is seen in diabetic rat hearts. Na+, K+ ATPase activity has also been shown to be depressed and the depression appears to correlate with depressed atrial contractility. High levels of circulating fats in diabetics may alter the integrity of membranes leading to altered enzyme activities. Insulin treatment has been relatively successful at reversing or preventing myocardial changes in the diabetic rat. Other treatments that have been studied include thyroid hormone treatment, since the depression of myosin ATPase can be corrected by such treatment; and carnitine treatment, as the elevation of long chain acyl carnitines (LCAC) and the resulting depression of calcium uptake in the SR can be so normalized. These treatments have not been successful at normalizing cardiac function. A combination of the two treatments normalized function only partially, suggesting that factors besides myosin ATPase and SR calcium uptake are involved. Other treatments that have been tried include vanadate, methyl palmoxirate, and choline and methionine. Vanadate treatment has proved to be encouraging in that it normalizes both function and hyperglycemia. Methyl palmoxirate, a fatty acid analog, normalized only the elevation of LCAC but did not affect function. Methionine and choline were only partially successful in preventing the functional alterations of diabetic rat hearts. The purpose of the present article is to review our understanding of diabetes-induced myocardial problems and their possible causes. Findings from our laboratory and others are described in which attempts have been made to normalize cardiac function.
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PMID:Diabetes-induced abnormalities in the myocardium. 293 41

The purpose of this study was to determine the coexistence of idiopathic hypertrophic cardiomyopathy (IHC) and atheromatous coronary artery disease. We studied forty six patients with IHC documented by complete clinical study and also by left heart catheterization. The diagnosis was considered established, when the patient had a significant left intraventricular pressure gradient (LIPG) and by angiographic and or echocardiographic demonstration of systolic anterior movement of the mitral valve and asymmetric septal hypertrophy. In 15 patients a selective coronary angiography was performed because ischemic myocardial disease was suspected. There were eight patients with significant atherosclerotic obstruction (greater than 75% narrowing). There was one vessel disease in 13%, two vessels in 37% and three vessels in 50% of the patients. The LIPG was 43 +/- 20 mmHg, the left ventricular and diastolic pressure (LVEDP) was 18 +/- 11 mmHg in patients with atheromatous disease and there was no significant difference with the patients with normal coronary arteries with LIPG 52 +/- 31 mmHg and LVEDP 21 +/- 9 mmHg. Our data demonstrate that ischemic heart disease in patients with idiopathic hypertrophic cardiomyopathy is related not only to increase of the cardiac mass and/or the ventricular wall stress, but in some of them atherosclerosis plays a role in its pathogenesis. Significant differences were found between the aged in both groups. In the patients who had coronary atherosclerosis the mean age was 54 years; on the other hand in the patients with normal coronary arteries the mean age was 44 years. This last fact could explain the high frequency of atherosclerosis in the older patients.
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PMID:[Obstructive hypertrophic myocardiopathy and coronary atherosclerosis]. 294 24

Cardiac transplantation for the treatment of end-stage congestive heart failure has been shown to be of benefit regardless of the etiology. With few exceptions, the evaluation of patients with end-stage heart failure is the same, regardless of the etiology. In those with cardiomyopathy not as a result of CAD, special attention must be given to exclude secondary causes of cardiomyopathy such as amyloidosis, hemochromatosis, and sarcoidosis, as well as generalized systemic illnesses that may also involve the heart, either secondary or hereditary, because special consideration must be given to these patients on a case-by-case basis to determine that there is no general systemic involvement of the illness that would preclude satisfactory rehabilitation after transplantation. Before cardiac transplantation becomes widely available, there must be a greater number of donor hearts, the lack of which now severely limits the number of transplants performed in comparison with the estimated need.66 Additionally, more effective and specific immunosuppressive agents must be identified in order to reduce the incidence of rejection, infection, and accelerated atherosclerosis that now limits the longevity of transplant recipients. Furthermore, the ideal immunosuppressive agent should be associated with fewer side effects than those currently available. The emotional and economic burdens placed on the patient, the family, and society must be balanced against the benefits generated by the procedure. Despite these limitations, cardiac transplantation continues to offer hope for the terminally ill patient, which must be tempered by an understanding of the real limitations of transplantation.
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PMID:Patient selection and results of cardiac transplantation in patients with cardiomyopathy. 304 84

Because hyperlipidemia may be a factor in the development of late graft atherosclerosis after heart transplantation, we have studied serum lipid levels in patients during the first year after transplantation. Serum cholesterol and triglyceride levels were measured in the preoperative period and at regular intervals up to 12 months after transplantation in 22 consecutive heart transplant recipients. Patients were divided into two groups: group 1 included 10 patients with underlying ischemic heart disease, and group 2 had 12 patients with underlying idiopathic dilated or valvular cardiomyopathy. Mean serum cholesterol concentrations in both groups increased substantially after operation and peaked at 3 months (respective rises of 35% and 30%). By 12 months after transplantation 50% of group 1 and 33% of group 2 manifested a significant degree of hypercholesterolemia (plasma cholesterol greater than 6.5 mmol/L, 250 mg/100 ml). Mean serum triglyceride concentrations increased in both groups during the latter part of the first year (respective increases of 44% and 13%). At 12 months only 10% of group 1 and 8% of group 2 manifested a significant degree of hypertriglyceridemia (plasma triglycerides greater than 3.0 mmol/L, 265 mg/100 ml). Over the first postoperative year there was a progressive increase in body weight, and this correlated highly with the increase in serum lipid levels (r = 0.90 for serum cholesterol and r = 0.84 for serum triglycerides). The role of conventional risk factors including hypercholesterolemia in the development of graft atherosclerosis remains uncertain, but until their role is defined, further strenuous efforts at weight control as a means of preventing or managing hyperlipidemia need to be explored.
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PMID:Hyperlipidemia after heart transplantation. 329 Mar 99

Cardiac transplantation represents an expanding therapeutic modality for end-stage heart disease in children and adolescents. During the past 5 years, 27 patients (15 boys; 12 girls) between the ages of 2 and 18 have undergone cardiac transplantation. The preoperative diagnosis was cardiomyopathy in 24 (six familial), congenital heart disease in two, and endocardial fibroelastosis in one. Immunosuppression included cyclosporine, azathioprine, and prednisone. There were 22 survivors, with four hospital deaths (three infection, one pulmonary hypertension), and one death at 4.5 years from graft atherosclerosis. The actuarial survival at 4 years was 83 +/- 7.4% and that at 5 years was 69 +/- 14.2%. Renal function was stable at 4 years, with an average creatinine clearance of 69.75 +/- 27.0 ml/min/m2. Hypertension was present in 21 of 22 patients, who require multiple drug therapy. Rehabilitation is 100% among discharged patients, with 14 in school, six employed, and two toddlers.
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PMID:Cardiac transplantation in children and adolescents. 331 54

SLE is an inflammatory disease of unknown etiology with the potential of affecting virtually all organ systems. Cardiovascular involvement occurs frequently, although it is often mild enough not to cause clinical concern. Pericarditis is most commonly subclinical, noted only on echocardiogram. Pericardial fluid, which can accumulate rapidly enough to cause tamponade, is inflammatory in nature and can totally mimic infection. The occurrence of Libman-Sacks endocarditis, usually a pathological diagnosis of little clinical significance, has little if any correlation with the presence of audible murmurs. However, valve replacement is occasionally necessary secondary to sterile destruction. These valvular lesions can also embolize or become infected. The incidence of ischemic coronary disease is increased, both secondary to premature atherosclerosis and, rarely, coronary arteritis. Conduction disease and arrhythmias are infrequently reported in adult patients, but congenital CHB has been noted in children born to mothers who have circulating anti-Ro antibody. Evidence is accumulating that suggests there is a mild cardiomyopathy associated with SLE that may be due to thrombotic or inflammatory microvascular coronary disease. Acute clinical myocarditis also rarely occurs. Therapeutically, at present, a reasonable course would seem to be to limit all known possible contributing factors to premature coronary artery and myocardial disease (hypertension, hypercholesterolemia, smoking, steroid therapy, etc), to be vigilant about recognizing the rarer complications associated with SLE (infectious pericarditis and endocarditis, coronary arteritis, pericardial tamponade, clinical myocarditis), and to remember that these uncommon complications are indeed uncommon. The importance of vigorously treating systemic hypertension cannot be overstressed.
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PMID:Cardiovascular involvement in systemic lupus erythematosus. 333 84

Two strains of obese rats, the fatty Zucker and the LA/N-corpulent have been compared at 6 months age for the presence of vascular and myocardial disease. Both strains, when obese, exhibit a VLDL hyperlipidemia with elevated triglycerides and moderate elevations of plasma cholesterol concentrations compared to the lean rats of the same strain. The hyperlipidemia is more modest in the fatty Zucker than the corpulent LA/N, and the serum lipid concentrations of the lean Zucker are lower than those of the lean LA/N. Apolipoprotein concentrations were similar and elevated in the two obese genotypes compared to the lean genotypes which were also similar to each other. Male and female obese animals of both strains exhibited hyperinsulinemia under fasting conditions and after oral glucose, with obese male LA/N rats exhibiting the most severe hyperinsulinemia. Glucose tolerance was impaired in obese LA/N animals but was normal in lean rats of both strains and fatty Zucker rats of both sexes. The glucose intolerance observed in obese LA/N animals was more severe in the male than in the female rats. Unlike the corpulent rat, which develops atherosclerotic lesions, the fatty Zucker shows no evidence of advanced vascular lesions on scanning electron microscopy. The fatty Zucker also does not develop the myocardial lesions that are frequent in the male corpulent LA/N rat. It is suggested that the initiation of the atherogenic process is dependent upon elevated insulin levels or transient hyperglycemia. Development of the advanced lesions appears to require the presence of hyperlipidemia.
Atherosclerosis 1988 Feb
PMID:Atherogenesis in two strains of obese rats. The fatty Zucker and LA/N-corpulent. 334 41

In order to evaluate Doppler echocardiography (DEC) used for cardiac output (CO) measurement, 22 patients (7 with coronary heart disease, 6 with dilatation cardiomyopathy, 5 with primary pulmonary hypertension and 4 with rheumatic heart disease) were studied. In all patients, invasive CO determination was performed by right heart catheterization, using thermodilution (T). In DEC, CO was calculated as CO = IV.S.HR, where IV was integral velocity, estimated on the basis of flow areas under planimetric curves, S was aortic root cross-section area, and HR was heart rate. A close correlation was demonstrated between DEC and T results (r-0.74). Only in one case with severe aortic atherosclerosis was there a significant difference between the data. This case excluded, the correlation becomes even closer (r-0.86). It is concluded that: 1) DEC is a valuable and precise method of CO assessment, 2) DEC may be used to monitor treatment efficacy, and 3) its limitation is aortic lesions.
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PMID:[Non-invasive evaluation of cardiac output by Doppler echocardiography]. 339 76

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.
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PMID:[Cardiological findings in acromegaly]. 343 27

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.
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PMID:Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy. 343 79


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