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

Uncontrolled hypertension increases the workload of the left ventricle causing the development of hypertrophy and an increase in myocardial oxygen consumption that may precipitate ischemia because of inadequate oxygen delivery related to accelerated coronary atherosclerosis. Control of the hypertension should prevent the further development of hypertrophy, delay the development of fibrosis and possibly also slow the rate of development of atherosclerosis. Furthermore, when myocardial function is impaired because of hypertrophy or other myocardial diseases, the level of blood pressure becomes an important determinant of left ventricular performance. Regardless of the level of arterial pressure, vasodilator drugs that lower arterial pressure may result in marked improvement in left ventricular performance and relief of symptoms of left ventricular failure. Therefore, control of blood pressure in the presence of heart disease may involve treatment of normotensive patients to bring them into a lower normotensive range as well as the more traditional treatment of hypertensives to bring them into the normotensive range. Although this scenario is consistent with conventional wisdom and clinical experience, intricacies of the relationship between hypertension, hypertrophy, myocardial oxygen delivery, atherosclerosis and intramyocardial blood flow distribution remain poorly understood. Until these aspects of the natural history of heart disease are better worked out therapy will remain largely empirical.
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PMID:Heart disease in the hypertensive patient. 14 Feb 80

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

We review the hemodynamic effects and clinical usefulness of five natural and synthetic catecholamines. Their actions are best understood by an appreciation of the relative ability of each catecholamine to activate alpha, beta 1 and beta 2 adrenergic receptors in the myocardium and peripheral vasculature. Epinephrine, the first catecholamine isolated, is shown to have little useful role in the therapy of acute myocardial infarction. L-norepinephrine has powerful alpha and moderate beta 1 effects. It is the catecholamine of choice in the initial treatment of cardiogenic shock associated with acute myocardial infarction. Isproterenol markedly increases myocardial contractility and heart rate by beta 1 stimulation, while simultaneously decreasing peripheral vascular resistance and, therefore, arterial pressure through its action on beta 2 receptors. It increases cardiac output, but its metabolic costs are high in the presence of ischemia. Its role in the therapy of acute myocardial infarction has largely been supplanted by more selective agents. Dopamine causes slightly less vasoconstriction than l-norepinephrine and slightly less myocardial stimulation than isoproterenol. In low doses, it increases renal and mesenteric blood flow by activation of a non-adrenergic receptor. Tachycardia and associated metabolic deterioration render it a second-line drug in the treatment of severe cardiogenic shock. Dobutamine, a new synthetic catecholamine, has primarily beta 1 activity. It increases myocardial contractility with little effect on heart rate or peripheral vascular resistance. It is ineffective in cardiogenic shock, but may eventually be shown to have a role in the treatment of left ventricular failure uncomplicated by severe hypotension.
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PMID:Use of catecholamines in acute myocardial infarction. 39 85

Nitroglycerin reduces ischemic injury during acute myocardial infarction (AMI) in dogs--an effect that is potentiated when drug-induced hypotension and tachycardia are prevented with phenylephrine. To determine the effectiveness of nitroglycerin, alone or with phenylephrine, during AMI in man, 12 patients (five or whom had left heart failure) were evaluated by summing ST-segment abnormalities (sigmaST) from 35 precordial electrodes. The seven patients without heart failure did not benefit consistently from nitroglycerin alone; however, addition of phenylephrine to abolish nitroglycerin-induced arterial pressure reduction uniformly diminished sigmaST (4.9 to 3.2 mv; P less than 0.05). In patients with heart failure, nitroglycerin alone consistently reduced ischemia (5.8 to 4.4 mv, P less than 0.05); addition of phenylephrine often partially reversed this effect. Thus, administration of nitroglycerin, alone or with phenylephrine, can reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends on the presence or absence of left ventricular failure before treatment.
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PMID:Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction. 80 12

This study was based on the concept that intracellular accumulation of calcium plays a role in mediating ischemic myocardial injury and that inhibition of entry of calcium into cells may have a salutary effect on the ischemic heart. Nifedipine, a potent vasodilator and inhibitor of transmembrane calcium flux, was infused into the aortic root of 6 dogs (5 microgram/kg/hr) during 2 hours of myocardial ischemia while on cardiopulmonary bypass. Seven control animals received normal saline at the same flow rate and temperature (20 degrees C). The results showed that none of the 7 control animals were able to maintain adequate aortic pressure or cardiac output after 30 to 60 minutes of normothermic reperfusion. All had marked left ventricular failure and were unresponsive to large doses of inotropic agents. In contrast, the 6 dogs treated with nifedipine were weaned from bypass either without difficulty or requiring small doses of calcium chloride and norepinephrine. Light microscopy demonstrated more marked ischemic damage in the control group than in the group of drug-treated dogs. We conclude that the concept of inhibition of transmembrane calcium flux offers a new and potent method for myocardial preservation during ischemia.
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PMID:Pharmacological preservation of the ischemic heart. 90 99

Fifteen postoperative surgical patients, in whom noncardiac pulmonary edema developed were studied. A presumptive diagnosis of left ventricle failure would have been based on historical evidence of heart disease (80%), electrocardiographic changes of ischemia or arrythmia (87%), or cardiogenic shock (20%). (see article) Fig. 6. PAEDP-PCW gradient. Note that arterial oxygen tension had an inverse relationship to this pressure differential. Roentgenographic findings included pulmonary edema (73%), pulmonary vascular congestion (60%), cardiomegaly or congestive heart failure (40%). Mean increase in A-aDO2 was 290 torr. Further cardiovascular investigation seemed to exclude left ventricular failure. Mean cardiac index was 4.1 plus or minus 1.3 L/min/m2; pulmonary capillary wedge pressure 4 plus or minus 2.7 torr, and stroke work was 87 plus or minus 8.7 gm-meters. Possible etiologic agents included elevated pulmonary artery pressure (67%), allergic reactions (27%), peritonitis or multiple system trauma (54%), or multiple transfusions (33%). Forty-seven per cent of the entire group survived. Therapy was directed toward the underlying noncardiogenic suspected etiology. Direct cardiovascular measurements were necessary to correct the erroneous though seemingly well founded suspected diagnosis of left ventricular failure in these patients.
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PMID:"Pseudocardiogenic" pulmonary edema. 111 52

The clinical and laboratory findings diagnostic of acute myocardial infarction include at least two of the following: (1) a history of pain consistent with myocardial ischemia, (2) electorcardiographic findings consistent with infarction, and (3) a rise in the serum level of specific cardiac enzymes. By the 4th or 5th day of illness, specific criteria can be applied to assign certain patients to a subset with "uncomplicated completed acute myocardial infarction." These criteria include the absence of evidence of (1) continuing cardiac ischemia, (2) left ventricular failure, (3) shock, (4) important cardiac arrhythmias, (5) conduction disturbances, and (6) other serious illnesses in patients with an established acute myocardial infarction. In terms of prognosis and management, patients in this subset should be regarded as substantively different from patients in other subsets. They should respond favorably to short periods of immobilization and hospitalization than those generally used. They may remain at bed rest (modified in regard to sitting and the use of a commode) for 4 days. Subsequently, mobilization with a program of progressive activity over the ensuing 5 to 10 days should reduce the duration of hospitalization to less than the current average of 17.5 to 20.8 days for patients with acute myocardial infarction. Nine to 14 days should suffice in most instances. Current and future trials may indicate that still earlier mobilization and shorter hospitalization periods can be applied to certain patient groups, but the evidence on this point is incomplete. For the individual patient, many factors will determine the optimal duration of bed rest and hospital stay. The patient's physician must consider the therapeutic benefits that may attend earlier mobilization and shorter hospitalization while weighing potential disadvantages. When the responsible physician does not regularly care for the patient, consultation with an experienced cardiologist is desirable. Patients whose condition is classified as "uncomplicated" may manifest deterioration during their illness and require assignment to a subset with a different prognosis and requiring different forms of treatment. For patients with uncomplicated acute myocardial infarction, as well as those in other subsets, absolute rules for therapy are unwise and application of broader principles by the alert physician is more likely to be beneficial.
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PMID:Duration of hospitalization in "uncomplicated completed acute myocardial infarction". An Ad Hoc Committee review. 125 73

One hundred consecutive aortic valve replacements were studied. Fifteen patients had a myocardial infarction as a result of the operation, and four of the five deaths in the series stemmed from this group. In the four deaths from infarction, autopsy revealed occlusion of a main coronary artery. This was attributable to coronary perfusion in three instances. All of the 11 survivors who sustained an infarct were free of angina and left ventricular failure 6 weeks after the operation. Patients with infarcts had longer bypass times and larger aortic systolic gradients than the patients who did not have an infarct. It is suggested that an infarct can occur as the result of occlusion of a main coronary artery; this is a fatal event commonly related to trauma from the coronary perfusion cannula. Alternatively, infarction may result from regional ischemia, perhaps without vessel occlusion, and is associated with long bypass times and with large aortic valve gradients. In such cases the prognosis is good. However, myocardial infarction was the major cause of death in this series.
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PMID:Myocardial infarction complicating aortic valve replacement. 127 36

The use of calcium antagonists for postinfarct cardioprotection remains controversial. Several major trials have failed to show benefit, despite positive expectations based on promising experimental data. A clue to the problem with the calcium antagonists was provided by the diltiazem trial, in which an adverse effect in the presence of congestive heart failure masked a benefit in those without heart failure. Accordingly, the most recent trial, DAVIT-II, was carried out in patients in whom preexisting left ventricular failure had been excluded. One of the interesting byproducts of that study was the possibility that verapamil prevented postinfarct sudden death, which implies a potential antiarrhythmic mechanism. It is proposed that cytosolic calcium overload could play a role in ischemic ventricular fibrillation. Experimentally, calcium antagonists are most effective antifibrillatory agents when catecholamine stimulation is combined with acute ischemia, as would be the situation in the acute phase of myocardial infarction. This potential benefit of calcium antagonists may be offset in the presence of congestive heart failure because left ventricular dilation is directly arrhythmogenic. The ideal calcium antagonist, aimed at preventing postinfarct ischemic arrhythmias, but without a significant negative inotropic effect, could be based on 1 of 2 principles. First, the agent could be highly selective for the ischemic but not the nonischemic zone of the myocardium (ischemic-selective agent). Second, the agent could be highly vascular selective, so that left ventricular dilation would be avoided. A comparative study of these two types of calcium antagonists should be undertaken in postinfarct patients.
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PMID:Should calcium antagonists be used after myocardial infarction? Ischemia selectivity versus vascular selectivity. 836 8

To better understand the factors predisposing a patient to death after elective percutaneous transluminal coronary angioplasty (PTCA) and to gain insight into indications for high-risk PTCA both with and without adjunctive use of support devices, the outcomes of 8,052 consecutive procedures were reviewed. Death occurred after 32 procedures (0.4%) and was directly related to coronary artery closure in 26 (81%) of these cases. Left ventricular failure due to vessel closure at the dilated site, the most common cause of death, was independently correlated with female sex (p less than 0.001), "jeopardy score" (p less than 0.001) and PTCA of a proximal right coronary artery site (p = 0.002), but not with left ventricular ejection fraction or presence of multivessel disease. Right ventricular failure after closure of the proximal right coronary artery, and left main coronary dissection accounted for the majority of the remaining deaths. Systolic blood pressure immediately after coronary artery closure was also closely correlated with jeopardy score, and cardiogenic shock was frequent in women with scores greater than or equal to 3.5 and in men with scores greater than or equal to 5.0. These data highlight the superiority of the jeopardy score versus ejection fraction in the determination of risk, stress the importance of gender in determining outcome and point to the need for better means of right ventricular protection from severe ischemia. Therefore, an initial framework for rational use of PTCA and support devices in the high-risk setting is established.
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PMID:Causes and correlates of death after unsupported coronary angioplasty: implications for use of angioplasty and advanced support techniques in high-risk settings. 174 25


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