Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D has been proposed as a risk factor of ischaemic heart disease. In 12 patients with acute myocardial infarction the major circulating vitamin D metabolite, 25-hydroxy-cholecalciferol (25-HCC), did not show any fluctuations during the first 4 days after onset of symptoms. The serum 25-HCC level was then measured in 128 patients consecutively admitted because of chest pain, 53 of whom had myocardial infarction and 75 had angina pectoris. The values found did not differ from those measured in 409 normal persons. The seasonal variations of serum 25-HCC were less pronounced in heart patients than in normals, probably due to less sun exposure in the summer months. The levels of serum 25-HCC did not correlate with the concentrations of serum cholesterol, glycerides, calcium or magnesium. Low serum calcium and magnesium were observed in all patients. Serum calcium was further reduced in the course of acute myocardial infarctions while serum parathyroid hormone rose significantly. We conclude that patients with ischaemic heart disease are not ingesting or producing in their skin elevated amount of vitamin D.
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PMID:Vitamin D and ischaemic heart disease. 74 75

Two women who had an acute myocardial infarction during the early postpartum period are described, and the findings in nine other women previously reported on are summarized. Attention is called to the atypical nature of ischemic heart disease and myocardial infarction in these patients when compared with myocardial infarction during pregnancy and with ischemic heart disease in men. Postpartum infarcts most often occur in women in their 20s during their first pregnancy, frequently a pregnancy complicated by the preeclampsia-eclampsia syndrome, and are associated with a high mortality rate. In one of our patients and one patient previously reported on, the results of coronary arteriography were normal, suggesting that coronary arterial thromboembolism or spasm was a cause of the infarction. Because postpartum myocardial infarction may be unrelated to atherosclerotic narrowing, detailed angiographic studies in such patients appear warranted. These cases indicate the variety and complexity of ischemic heart disease in women.
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PMID:Postpartum acute myocardial infarction: a rare occurrence of uncertain etiology. 75 60

Scintigraphic, clinical and pathological findings were correlated in 52 patients studied by technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigraphy before death or surgical resection of myocardium. Fifty-nine clinical events were studied with scintigraphy in the 52 patients; 41 of the 59 were associated with one or more abnormal 99mTc-PYP studies and 18 with normal 99mTc-PYP scintigrams. Myocardial scintigrams were positive in 29 of 31 cases with clinicopathological evidence of a corresponding discrete, grossly obvious acute myocardial infarct, including 16 of 16 transmural myocardial infarcts and 13 of 15 subendocardial infarcts. In 16 of 18 cases, negative myocardial scintigrams correlated with the absence of acute myocardial infarction determined by clinicopathological evidence. In two cases small subendocardial infarcts (less than 3 g) were not detected by 99mTc-PYP myocardial scintigraphy. Of the 12 additional instances of positive 99mTc-PYP myocardial scintigrams, five were associated with clinical unstable angina pectoris and seven were in the category of persistently positive scintigrams, since the scans were obtained 2.5 months or longer after proven or suspected acute myocardial infarcts. In all 12 instances, the positive 99mTc-PYP scintigrams were associated with evidence of multifocal irreversible myocardial damage consisting of myocytolysis, coagulation necrosis and/or fibrosis, and the histological age of the lesions was compatible with acute injury corresponding to the time of scintigraphy. The findings indicate that a positive 99mTc-PYP myocardial scintigram is a sensitive indicator of significant myocardial injury which may occur as confluent coagulation necrosis corresponding to clinical acute myocardial infarction, or as multifocal coagulation necrosis or myocytolysis associated with unstable angina pectoris or recurrent ischemic heart disease, especially after previous infarctions.
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PMID:Clinicopathologic findings in 52 patients studied by technetium-99m stannous pyrophosphate myocardial scintigraphy. 75 94

1329 patients were discharged alive after acute myocardial infarction initially treated in a CCU. In a five-year follow-up, 537 (40%) of the patients died. Routine data registered uniformly during the CCU period showed that, apart from age, the most important factors regarding long-term prognosis in general were previous ischaemic heart disease and direct or indirect signs of heart failure registered in the CCU. The possibilities to predict sudden death (130 patients died within 2 hours of onset of final symptoms during the follow-up period) were small, although a definite dominance of this mode of death was noted in patients below 60 years of age. The clinical profile of the majority of the 134 patients who died during the first half-year was distinguished by a history of prior myocardial infarction and signs of left heart failure during the CCU stay. However, in a significant number of patients dying early after discharge, none of the ordinary unfavourable prognostic signs had been registered.
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PMID:Early and sudden deaths after myocardial infarction. A report from the Swedish CCU study. 76 Apr 5

To reduce myocardial ischemia effectively, mechanical or surgical interventions must achieve either augmentation in coronary blood flow, a reduction in myocardial oxygen demand, or a combination of both. Coronary bypass graft procedures can achieve an immediate augmentation in coronary blood flow distally through the involved vessel and thereby improve myocardial perfusion and oxygen delivery and thus have the potential for reversing myocardial ischemia both acutely and for the long term. Although myocardial revascularization may resolve the ventricular functional alterations associated with acute myocardial ischemia it remains uncertain whether revascularization can reverse ischemic myocardial cellular injury and in what time framework, as related to reversible vs. irreversible ischemic cellular changes. Mechanical circulatory assistance (MCA) using diastolic counterpulsation effectively reduces myocardial ischemia by the physiologic mechanisms of 1) decrease in left ventricular after-load and left ventricular wall tension, 2) improvement is cardiac output by diastolic counterpulsation and 3) augmentation of coronary blood flow by diastolic pressure augmentation. The most effective indication for either MCA or myocardial revascularization is for interruption of myocardial ischemia prior to the development of infarction. Clinical sudies have demonstrated that acute myocardial ischemia can be effectively interrupted by intraaortic balloon pumping (IABP) including reversal of left ventricular dysfunction associated with acute myocardial ischemia. In most instances, cessation of IABP resulted in recurrence of myocardial ischemia indicating the need for urgent revascularization surgery. In the management of medically refractory myocardial ischemia. IABP has been effective in complete suppression of ischemia in 80 percent and resulted in marked improvement in all, allowing safe revascularization surgery with an operative mortality in the range of 5% and perioperative myocardial infarction incidence of 2%. In patients with acute myocardial infarction and cardiogenic shock (AMI-CS), IABP can resolve CS in 75 percent. The combination of IABP and surgery has resulted in survival approaching 45 percent indicative of a significant improvement in salvage in this group of patients where expected mortality approaches 100 percent.
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PMID:Mechanical and surgical interventions for the reduction of myocardial ischemia. 76 16

Alterations of autonomic tone appear to have important effects on the electrical stability of the heart. Since altered electrical stability, ventricular fibrillation, is the cause of death in the majority of patients who die from ischemic heart disease, the effects of the autonomic nervous system on ventricular electrical stability have been examined. Increased vagal tone increases the electrical stability of the heart and reduces the incidence of spontaneous ventricular fibrillation after coronary occlusion. These salutary effects of increased cholinergic tone appear to be mediated by cholinergic innervation of the ventricular conducting system. Conversely, increased adrenergic tone decreases the electrical stability of the heart and increases the propensity of the heart to develop ventricular arrhythmias during coronary occlusion. The interaction of the adrenergic and cholinergic system during myocardial ischemia may be one of the important determinants of survival in patients with coronary artery disease and acute myocardial infarction.
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PMID:Neural basis for the genesis and control of arrhythmias associated with myocardial infarction. 78 2

Under observation were kept 80 patients with signs pointing to the sick sinus syndrome. Most of them suffered from ischemic heart disease, from atherosclerotic cardiosclerosis and acute myocardial infarction. Persistent sinus bradycardia with active and passive heterotopic arrhythmias were recorded in 42 patients. Sino-auricular block of the II and III degrees or asystolia of the atria with ectopic arrhythmias were observed in 37 cases. A number of patients displayed fibrillary bradyarrhythmia, extrasystole with post-extrasystolic depression of the rhythm and other disturbances. The so-called tachycardia-bradycardia syndrome characterized by the presence of tachycardiac arrhythmias occurring against the background of a marked bradycardia was registered in 25 persons. Fifteen patients demonstrated attackes of the Morgagni-Adams-Stokes syndrome, usually associated with lengthy periods of cardiac asystole. The treatment of ectopic arrhythmias in patients with the sick sinus syndrome presents considerable difficulties, but in many of them these disorders could be successfully eliminated by a careful and rigidly controlled application of antiarrhythmic agents (isoptin, ajmalin, pulsnorma, rhythmodan, beta-adrenergical blocking agents). For some patients exhibiting a tendency toward asystole electric stimulation of the heart is indicated.
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PMID:[Syndrome of sino-atrial node asthenia]. 79 80

Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.
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PMID:Intravenous nitroglycerin in acute myocardial infarction. 80 31

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.
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PMID:Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease. 80 82

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agnet in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (less than or equal to 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (greater than 12 MM Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 TO 7 MM Hg; P less than .01), mean systemic arterial pressure (MAP) (95 TO 82 MM Hg; P less than .01), cardiac index (CI) (1.79 TO 1.46 L/min/m-2; P less than .02), stroke index (SI) (24 TO 18 CC/M-2; P less than .01) and stroke work index (SWI) (27 TO 20 GM TIMES M/M-2; P less than .01). These alterations were significant in both subgroups, with the decline in PAW greater (P less than .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline ofpump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accomppanied by potentially deleterious fall in cardiac output and systemic blood pressure.
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PMID:Hemodynamic effects of nitroglycerin in acute myocardial infarction. 80 94


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