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

The effectiveness of the calcium antagonist nifedipine in preserving postischemic myocardial function and structural integrity was experimentally demonstrated in isolated rabbit hearts, in conscious dogs subjected to myocardial infarction, in open chest anesthetized dogs with normothermic regional ischemia induced for 1 to 2 hours and in dogs undergoing hypothermic global ischemia for 2 hours followed by 2 hours of reperfusion. Nifedipine had a beneficial effect on postischemic myocardial stiffness and mitochondrial calcium accumulation, which were correlated. Administration of nifedipine at the onset of myocardial infarction increased blood flow to ischemic zones of myocardial infarction and resulted in less loss of creatine kinase. It reduced by two- to three-fold the volume of the ischemia-reperfusion injury induced by left anterior descending coronary arterial occlusion and release and preserved indexes of hemodynamic function. Nifedipine was found effective in protecting myocardial performance and structure after 2 hours of global ischemia during hypothermic cardiopulmonary bypass. It is suggested that this agent may be useful as an adjunct to cold cardioplegia in man for enhanced myocardial protection during cardiac surgery.
Am J Cardiol 1979 Oct 22
PMID:Nifedipine: a myocardial protective agent. 49 88

The precise mechanism responsible for early contractile failure after the onset of myocardial anoxia or ischemia has attracted speculation and controversy. The simple and attractive hypothesis that adenosine triphosphate (ATP) deficiency is responsible for this failure has often been dismissed on the basis of claims that there is only a small reduction in cell ATP content at a time when contractile activity is severely reduced. The premise of this article is that the changes in cell ATP content and distribution that theoretically should occur after oxygen depletion may not have been adequately considered and that previous measurements of cell ATP content may not have been carried out at the correct time. Using an isolated rat heart preparation and high speed freeze-clamping techniques it has been possible to demonstrate that a substantial decrease in myocardial ATP and creatine phosphate content occurs after the onset of anoxia but before the onset of contractile failure. Thus, during the first 5 seconds of anoxia contractile activity remains constant whereas ATP decreases by 25 percent and creatine phosphate by 50 percent. Thereafter, contractile failure occurs and the rate of utilization of high energy phosphates declines with the cell content at a plateau or possibly increasing. These results are assessed in the light of the dynamic changes in energy metabolism occurring in early anoxia and suggest that ATP depletion in a specific cell compartment may be the primary trigger for early contractile failure.
Am J Cardiol 1979 Nov
PMID:Oxygen deprivation and early myocardial contractile failure: a reassessment of the possible role of adenosine triphosphate. 49 6

Patients with chronotropic incompetence, defined as a failure of the heart rate response to exercise to rise to within two standard deviations of the expected increase with exercise, where studied and compared to patients with known coronary disease by angiogram with and without ST segment depression. 72% of the patients with chronotropic incompetence but without ST depression had significant coronary heart disease. The demonstration of chronotropic incompetence in exercise testing has important predictive implications and should be looked upon as carefully as ST segment changes. There was no evidence of SA node ischemia in these patients. Intrinsic heart rate measurements done in this study suggest autonomic dysfunction as a possible pathophysiologic mechanism for chronotropic incompetence. The heart rate response to exercise may be a useful predictor of the presence and severity of coronary disease. Therefore, a predicted heart rate response with standard deviation for age and sex should be included as part of the stress test protocol.
Clin Cardiol 1979 Feb
PMID:Chronotropic incompetence in exercise testing. 49 1

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
Am J Cardiol 1979 Dec
PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

The effect of repeated local ischemia and reperfusion on myocardial metabolism and ventricular performance was studied in 12 open-chested pigs fasted overnight. Myocardial ischemia was induced by reduction of the flow in the left anterior descending coronary artery to 40% of control during 30 min. After 35 min of reperfusion a second 30-min occlusion period was started, again followed by a 35-min reperfusion period. At the end of both reperfusion periods coronary flow and coronary resistance had returned to control values. During control there was lactate uptake, but no significant uptake of glucose, free fatty acids (FFA), triglycerdies, glycerol and inosine. During the first occlusion period the heart released lactate and inosine, and used glucose and FFA. At the end of the first reperfusion period lactate uptake approached control values, but inosine was still released by 10 of the 12 animals. In the second ischemic period, glucose and FFA were again taken up. Lactate and inosine were released, but the production was much smaller than during the first occlusion period. Depletion of myocardial glycogen and high-energy phosphates could be responsible for this quantitatively different response. Necrosis may have played a role, although enzyme release was minimal and only observed after the second occlusion period. Heart rate, peripheral resistance and ventricular filling pressure were virtually unchanged throughout the course of the experiments. Maximum rate of fall of left ventricular pressure (min LVdP/dt) decreased during ischemia and did not recover during reperfusion. Changes in min LVdP/dt and cardiac output were more closely related than changes in max LVdP/dt and cardiac output. This model cannot be used for the study of interventions during myocardial ischemia in which the animal serves as its own control.
Basic Res Cardiol
PMID:Myocardial substrate utilization and hemodynamics following repeated coronary flow reduction in pigs. 52 55

This study was undertaken to examine the relationship between electrographic ST-elevation and regional myocardial blood flow during graded coronary constriction. Electrograms from the epicardial surface, outer and inner layers of the myocardium were recorded. Regional blood flow to the outer and inner layers of the myocardium was measured by means of a heat-clearance method. With the application of a coronary constriction, myocardial blood flow to the inner layer began to decrease with a 75% coronary constriction, while flow to the outer layer was maintained at near normal up to least an 80% coronary constriction. Non-linear squares curve of between ST-elevation and the decrease in myocardial flow resulted in y = 18.80 exp-0.06x - 0.02 in the outer layer and y = 9.22 exp-0.02x - 1.54 in the inner layer. Also the non-linear squares curve of between epicardial ST-elevation and the decrease in myocardial flow resulted in y = 50.91 exp-0.11 x + 0.04 in the inner layer and y = 10.29 exp-0.07 x + 0.03 in the outer layer. The standard deviations of the coefficients of the latter two equations were higher than those of the former two equations. The higher values indicated larger variations of the parameter coefficients and data points. These results clearly demonstrated that a regional intramyocardial electrogram more closely reflects local ischemia than does an epicardial electrogram.
Basic Res Cardiol
PMID:Relationship between epicardial and intramyocardial ST-segment voltage and myocardial blood flow during graded coronary constriction in the dog. 52 58

This investigation was undertaken in order to experimentally reassess the value of myocardial waviness and stretching as early histological indicators of acute myocardial infarction. Twenty three dogs were subjected to periods of ischemia, from 30 minutes to 4 hours; wavy fibers were present in 87% and 91% of the ischemic and non-ischemic samples respectively. It is concluded that myocardial fiber waviness lacks significance as an indicator or early myocardial infarction, whose diagnosis remains a major challenge.
Arch Inst Cardiol Mex
PMID:[Experimental reevaluation of myocardial ondulations in the early histological diagnosis of myocardial infarct]. 54

The effect of verapamil on ST changes was evaluated in 10 selected patients with acute myocardial infarction admitted to the Coronary Care Unit within 8 hours after the onset of symptoms. To evaluate the extent of ischemia it has been used the magnitude and direction of the ST vector derived from X, Y and Z leads of the Frank vector system. After a control period of 2 hours, during which the changes of the ST vector magnitude were assessed, each patient received 0.1 mg/Kg verapamil intravenously, ST vector magnitude (STVM), ST azimuth (STAZ), ST elevation (STEL), heart rate, systemic blood pressure and pressure-rate product were assessed 5, 15, 30, 45, 60, 75, 90, 105 and 120 minutes after the administration of the drug. Verapamil produced a significant progressive decrease in STVM (from a mean of 254 +/- 44 muV at the end of the control period, to 139 +/- 25 muV after 2 hours; P < 0.01). Systolic blood pressure decreased significantly throughout the trial; the most significant decrease was registered immediately after the infusion of verapamil (from a mean of 134 +/- 3 mmHg to 121 +/- 3 mmHg; P < 0.001). Pressure-rate product declined slightly. No significant change in STVM was observed in 10 control patients with acute myocardial infarction examined over a 4 hours period. The apparent protective effect of verapamil in myocardial ischemia is discussed in relation to its calcium-antagonistic properties in excitable tissues.
G Ital Cardiol 1979
PMID:[Effects of acute infusion of verampil on the ST segment elevation measured with the Frank orthogonal leads in patients with acute myocardial infarct]. 54 89

The effect of collateral circulation on regional myocardial flow and wall motion of left ventricle was studied on 5 anesthetized dogs with a surgically implanted constrictor on the left circumflex coronary artery (LC). The grade of LC stenosis and wall motion of left ventricle (LV) were determined by cineangiography of the coronary artery and LV at the period of acute and chronic occlusion. Regional myocardial flow was determined by tracer microspheres (TM), labeled with four different isotopes, Sr85, Cr51, Sc46, Ce141. The first TM1 was infused after LC stenosis, TM2 during a temporary complete LC occlusion at the period of acute occlusion; TM3 and TM4 in a similar way 3 to 4 weeks after the acute LC stenosis. Three to four weeks after LC stenosis, i.e. chronic period of occlusion, the degree of LC stenosis progressed from 70--80% to 100% occlusion, but collateral flow and collateral vessels to the ischemic LC area were increased together with an improvement of wall motion of the ischemic LC area. The results may support the idea that collaterals may be an effective compensatory mechanism for ischemia. In contrast to an increase of collateral flow to the ischemic LV free wall in all five dogs, an increase to the posterior papillary muscle was found only in two out of five dogs.
Basic Res Cardiol
PMID:Effects of collateral circulation on regional myocardial blood flow and left ventricular wall motion (A preliminary note). 58 2

99mtechnetium diphosphonate was used in 81 patients for myocardial imaging. 46 of the patients suffered, 2-6 days prior to the test, from an acute transmural infarction provided by clinical, ECG, and enzymatic evidence; the scintigram was definitely positive in 43, equivocal in 2, and negative in 1. In 16 patients with subendocardial infarctions, in 9 the scintigram showed a positive result, in 1 it was equivocal, and in6 patients negative. In 6 other patients who suffered from acute chest pain, followed by enzyme changes, but no ECG evidence of infarction throughout the hospitalization period, the scan was positive in all. In 13 patients with acute ischemia (unstable 'crescendo' angina), 9 had a positive, 1 an equivocal, and 3 a negative scan. We conclude that radionuclide imaging is a valuable addition to the methods already available for diagnosis of myocardial infarction. With the use of diphosphonate as the tracer, we found that acutely ischemic myocardium that later may recover, gives also positive imaging.
Eur J Cardiol
PMID:Radionuclide imaging of the heart in myocardial infarction and acute ischemia by 99mtechnetium diphosphonate. 59 Feb 93


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