Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.
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PMID:Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes. 9 18

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

This review consists of two parts: (1) discussion of the electrophysiologic mechanisms that are believed to produce ventricular repolarization changes during the electrocardiographic stress test, and (2) clinical assessment of the electrocardiographic changes with stress in patients with an abnormal electrocardiogram at rest. In the first part, the mechanisms of S-T segment elevation, S-T segment depression, T wave changes and linked S-T and T wave changes are reviewed. In the second part, all electrocardiographic abnormalities at rest are grouped into four categories: (1) changes that mask the manifestations of ischemia, (2) changes that stimulate or exaggerate the manifestations of ischemia, (3) changes that have no important effect on the manifestations of ischemia, and (4) changes that reproduce the patterns of acute myocardial infarction after an apparent healing. The reported studies of electrocardiographic stress testing in patients who have abnormal electrocardiogram at rest are summarized.
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PMID:Exercise testing for detection of myocardial ischemia in patients with abnormal electrocardiograms at rest. 14 9

Radionuclide techniques that assess regional myocardial perfusion and detect acute myocardial infarction promise to provide critical information in the detection and evaluation of coronary artery disease and in the assessment of therapies aimed at limiting the degree of ischemia and the extent of tissue necrosis. Radioindicators such as 99mTc-tetracycline and 99mTc-pyrophosphate which are sequestered by acutely infarcted myocardium provide a direct method to detect an infarct and to determine its size. Regional alterations in myocardial perfusion can be assessed by myocardial scintigraphy performed after the injection of radiopotassium or one of its analogues with the patient either at rest or at exercise. A somewhat more accurate evaluation of the extent of altered perfusion can be obtained after the intracoronary injection of macro-aggregated particles. A quantitative index of altered perfusion can be obtained after the intracoronary injection of an inert gas such as 133Xe.
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PMID:Radionuclide methods in the evaluation of myocardial ischemia and infarction. 17 72

Although acute infarction of the myocardium is known to accumulate 99mtechnetium pyrophosphate, it is not entirely clear that ischemia alone without necrosis does not result in abnormal uptake of 99mtechnetium pyrophosphate. The present study investigates whether transient myocardial ischemia is associated with localization of 99mtechnetium pyrophosphate by evaluating images obtained with the scintillation camera at rest and after exercise in 15 patients with unequivocal myocardial ischemia. All patients had angina pectoris, multivessel coronary artery stenoses by selective arteriographic studies, and electrocardiographic ischemic responses on treadmill exercise. Eleven of the 15 patients also underwent radionuclide imaging with 81rubidium at rest and after exercise; the results demonstrated scintigraphic ischemia. The scintiscans with 99mtechnetium pyrophosphate revealed no evidence of increased myocardial radioactivity after exercise compared to rest in 14 of the 15 patients. In contrast, myocardial activity was observed with 99mtechnetium pyrophosphate after treadmill exertion in the remaining patient, in whom a small subendocardial infarction appeared to have occurred with the exercise. It is concluded from these results that transient myocardial ischemia does not cause localization of 99mtechnetium pyrophosphate. These findings support the specificity of abnormal localization of 99mtechnetium pyrophosphate for acute myocardial infarction.
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PMID:Evaluation of myocardial uptake of 99mtechnetium pyrophosphate in clinical exercise-induced ventricular ischemia. 18 75

To clarify the value of serum enzymes in the detection of intraoperative and postoperative myocardial injury associated with coronary artery bypass grafting, we evaluated 70 consecutive patients (151 grafts). We used electrocardiograms and serial determinations of serum levels: serum glutamic oxaloacetic transaminase (SGOT), creatinine phosphokinase (CPK), lactic dehydrogenase (LDH), and LDH isoenzymes on Days zero, 1, 3, 5, 7, and 10. Patency of all grafts 1 week postoperatively was 92 per cent. Fourteen patients (20 per cent) had ECG evidence of acute myocardial infarction (AMI) or ischemia lasting longer than 48 hours. This incidence of AMI was attendant with no deaths or discernible changes in postoperative ventriculography. LDH-1 (cardiac fraction) was elevated in all patients with myocardial injury. Late elevation of LDH-1 occurred in 2 patients at the time of postoperative catheterization, 1 of whom had negative findings on ECG. Diagnostic correlation was not observed with total LDH, CPK, or SGOT. Predisposing factors to AMI included preinfarction angina (4 of 14 patients), occluded grafts (4 of 14), and a bypass time greater than 120 minutes.
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PMID:Myocardial injury and bypass grafting. Value of serum enzymes in diagnosis. 24 Sep 85

In order to determine the natural evolution of different clinical types of "unstable angina", 167 patients were included in a prospective study. After angiography, 11 (6.5%) were excluded because they had no significant coronary lesions. The remaining 156 were sorted into different groups according to their clinical characteristics and were followed up for a period of 24 months at least. After that follow-up period, mortality and incidence of acute myocardial infarction (AMI) were as follows: angina of recent onset (Class III--IV NYHA): 8.5% (3/35) and 34.2% (12/35). Progressive angina: 7.4% (2/27) and 7.4% (2/27). Intermediate syndrome: 41.6% (10/24) and 37.5% (9/24). Prinzmetal's angina: 10% (1/10) and 10% (1/10). Post acute myocardial infarction angina: 35% (7/20) and 10% (2/20). Acute persistent ischemia: 2.5% (1/40) and 20% (8/40). Comparison of these figures pointed out significant differences (p less than 0.001 for mortality and p less than 0.03 for AMI incidence respectively). We conclude that it is clinically possible to identify different groups within the so-called unstable angina. Such a division not only allows for the creation of more homogeneous groups, but it contributes to a more rational therapeutic approach and also permits identification of high risk prodromes of greater complications, such as myocardial infarction or sudden death.
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PMID:Clinical spectrum of "unstable angina". 26 65

A 65 years old woman with an acute myocardial infarction, as it was judged by serial enzyme changes, developed transitory Q waves in V2-V4 and II, III and AVF during the attack of chest pain. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle system. This defect could explain the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.
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PMID:Transient abnormal Q waves during acute myocardial infarction. 31 75

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.
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PMID:Echocardiography in ischemic heart disease. 32 1

Two grams of methylprednisolone was administratered to ten patients with acute myocardial infarction at an average of 13 hours from the onset of symptoms; pain in the chest was not relieved in six of the ten patients. In one hour, no significant improvement was noted in the function of the ischemic segments (examined using a multiaxis echocardiographic method) or in the S-T segments of the 12-lead electrocardiogram. Left ventricular filling pressure soon increased by an average of 4 mm Hg (P less than 0.005), without ventricular dilatation or a Frank-Starling response, suggesting a decrease (ischemic?) in myocardial compliance. Cardiac output by Swan-Ganz thermodilution later increased by 21 percent (P less than 0.01) when a decrease in peripheral vasoconstriction was evident. In contrast, small-dose beta-adrenergic blockade using 0.2 mg of pindolol intravenously after administration of methylprednisolone immediately relieved pain in the chest in all six patients. Elevation of the S-T segments was reduced by 34 percent (P less than 0.05) within 15 minutes, and the contractile function of the ischemic segments improved markedly, by 3 mm or to 34 percent of normal, from the 4 percent of normal before administration of pindolol (P less than 0.005). Hemodynamic function did not deteriorate in the eight patients with uncomplicated infarction or moderate left ventricular failure. Therapy with pindolol thus reduced clinical, electrocardiographic, and myocardial mechanical signs of acute ischemia safely, while administration of methylprednisolone had no short-term protective effect.
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PMID:Failure of methylprednisolone to protect acutely ischemic myocardium: a contrast with subsequent beta-adrenergic blockade in man. 34 14


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