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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

Evaluation of the concentration of atrial natriuretic peptide, angiotensin P, renin activity in the blood of the coronary sinus and aorta in 18 patients with IHD and hypertrophy of the left ventricle during development of induced ischemia revealed that in left ventricular hypertrophy secretion of atrial natriuretic peptide by the myocardium is reduced. The level of this reduction depends on the kind of hypertrophy. Dilatation of the left ventricle cavity furthers exhaustion of the secretory function of the ischemic myocardium.
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PMID:[The interrelation of the secretory activity of the myocardium with its hypertrophic characteristics in patients with ischemic heart disease]. 129 16

Six patients (2 males and 4 females, mean age of 46 years) with X syndrome were reported in this paper. All patients presented with typical exertional angina pectoris. In 4 patients the angina had a variable threshold of onset, it often occurred at rest and occasionally nocturnally. The electrocardiogram during chest pain showed ST segment depression of more than 0.05-0.1 mV in all 6 patients. The treadmill or bicycle ergometer exercise test was positive in 4 cases (ST segment depression > 0.1 mV), equivocal in 1 (ST segment < 0.1 mV) in whom the 201Tl exercise myocardial perfusion scan showed sign of ischemia, and negative in 1 in whom atrial pacing at heart rate of 135 beats/min induced angina and ST segment depression of 0.1-0.15 mV. Echocardiograms and X ray chest films revealed no sign of ventricular hypertrophy or enlargement. The 201Tl exercise myocardial perfusion scan was performed in 5 patients, which showed signs of ischemia in 4 patients and suspected to have ischemia in 1. Left ventriculograms and coronary angiograms were normal in all 6 patients. Ergonovine provoking test (total dose of 0.4 mg) was negative in 5 patients, it was not performed in 1 in whom there was no evidence of coronary artery spasm by angiogram during appearance of electrocardiographic ischemic changes and chest pain. Left ventricular endomyocardial biopsy was performed in 1 patient, which showed significant smooth muscle cell proliferation in the medial layer of a small artery with diameter of 62.5 mu which produced narrowing of the lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[X syndrome--report of six cases]. 130 21

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.
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PMID:Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit. 138 26

Altogether 58 patients suffering from arterial hypertension (AH) were examined. The patients with left ventricular hypertrophy (LVH) and changes in the ST-T demonstrated a high correlation between an increase of the end systolic tension (EST) and interval elongation and the minimal size of the left ventricle before mitral valve opening. These data point to the development of "high-stressful LVH" which is accompanied by a non-proportional increase of EST, subendocardial ischemia of the myocardium (changes in the ST-T) and derangement of diastolic heart function.
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PMID:[The nature of the changes in the repolarization complex of the ECG in patients with arterial hypertension and left ventricular hypertrophy]. 144 Mar

Unknown is the significance of the abnormalities of repolarization observed at rest in patients with coronary artery disease (CAD) demonstrated by coronary angiography, except for ischemic episodes, myocardial infarction, left ventricular hypertrophy, electrolyte changes or pharmacological interactions. The chronic T wave inversion and ST segment depression are usually considered as an alteration due to ischemia ("chronic myocardial ischemia"); this definition is, in our opinion, erroneous, because myocardial ischemia is an acute episode caused by a sudden lack of balance between demand and availability of myocardial oxygen, corresponding to transient electrocardiographic alterations. Thus, the definition of "chronic myocardial ischemia" referred to stable abnormalities of repolarization is incorrect, because a "chronic" lack of balance between MVO2 and O2 availability would produce necessarily irreversible myocardial damage (necrosis). To contribute to the comprehension of the stable ECG changes at rest, we have selected a group of patients with CAD demonstrated by coronary angiography, presenting stable T wave alterations and ST depression at rest. We have studied the main and regional left ventricular function through radionuclide angiocardiography (ACS). Comparing the abnormalities of repolarization (ECG) on the one hand with angio, EFR and VER on the other, we have obtained different positive correlations, according to the functional parameters considered (EFR and VER). In our study, the lowest positive correlation has been noticed comparing ECG versus angio, VER and EFR (37.5%), while the highest correlation was obtained when ECG was considered versus angio and VER (56.25%). Evaluating ECG versus angio and EFR we have obtained a positive correlation equal to 43.75%. So we have deduced that VER is the functional parameter that better relates to angio and ECG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A critical review of the stable changes in ventricular repolarization in ischemic cardiopathy. A correlation with the angiographic findings]. 148 33

The hypertrophied left ventricle is at considerably greater risk for injury when subjected to global ischemia than is an otherwise normal heart. We evaluated the efficacy of verapamil, a calcium-channel blocking agent, as an adjunct to standard crystalloid cardioplegic solution in animals with left ventricular hypertrophy subjected to myocardial ischemia during cardiopulmonary bypass. Infracoronary aortic stenosis was produced in 15 mongrel puppies by plication of the noncoronary cusp of the aortic valve. Studies were conducted 3 to 4 months later. Left ventricular catheter-tip pressure transducers and major and minor axis ultrasonic dimension crystals were inserted, and the animals were then supported by cardiopulmonary bypass with 30 minutes of normothermic ischemia. Animals were randomized to receive either standard hyperkalemic crystalloid cardioplegic solution (n = 8) or the same solution with verapamil, 0.1 mg/kg (n = 7). After the 30 minutes of ischemia, the animals were supported on cardiopulmonary bypass for an additional 30 minutes and then separated from bypass. They were then studied for another 2 hours by measurement of myocardial adenosine triphosphate content, myocardial blood flow, systolic function with use of the end-systolic pressure/volume ratio, and compliance with use of the natural strain coefficient of the minor axis at 15 mm Hg end-diastolic pressure. There was a better recovery of systolic function in the animals treated with verapamil (89.2% versus 63.3%). The compliance as measured with use of the minor axis natural strain coefficient returned essentially to baseline in the group of animals treated with verapamil (0.236 +/- 0.038 before ischemia and 0.254 +/- 0.043 2 hours after ischemia), but it fell markedly in the control animals (0.219 +/- 0.027 before ischemia and 0.153 +/- 0.016 2 hours after ischemia). Myocardial adenosine triphosphate levels were not significantly different at any time during the study. Likewise, myocardial blood flow was not significantly different between groups. We conclude that the addition of verapamil to hyperkalemic cardioplegic solution improves recovery of both systolic and diastolic function after global ischemia in dogs with left ventricular hypertrophy resulting from aortic stenosis. The precise mechanism for this is unknown.
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PMID:Response of the hypertrophied left ventricle to global ischemia. Comparison of hyperkalemic cardioplegic solution with and without verapamil. 153 56

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.
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PMID:Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs. 153 67

We examined the effect of age on capacity for myocardial hypertrophy, pressure-generating ability and coronary circulation after imposition of pressure-overload. Marked right ventricular and cellular hypertrophy was observed 1 week after pulmonary artery constriction in the developmental phase of rats (2 months of age) and after 3 weeks in the young-adult rats (7 months). In old rats (18 months) similar increases in peak right ventricular pressure did not produce significant hypertrophy even after 3 weeks. The right ventricular hypertrophy at the organ and cell levels in response to pressure-overload decreased with age. In vivo pressure-generating ability, which was determined by maximum isovolumic pressure during pulmonary artery occlusion, correlated with the degree of myocardial hypertrophy in each age group. During the ascending aortic constriction experiment the age-associated diminution in hypertrophic response was also observed in the left ventricle. Coronary dilator capacity, which was determined after brief ischemia in an isolated, blood-perfused, beating but nonworking heart model, was decreased in the presence of myocardial hypertrophy in young-adult rats (7 months) and in the absence of significant myocardial hypertrophy in old rats (18 months). The age-associated diminution in capacity for myocardial hypertrophy, pressure-generating ability and maladaptation in the coronary circulation may explain the higher incidence of heart failure or increased vulnerability of the myocardium to ischemic episodes during hemodynamic stress in aged patients.
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PMID:Aging effects on myocardial hypertrophic response and coronary circulation in pressure-overload. 153 57


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