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

Increasingly longer balloon inflation times during coronary angioplasty can create significant left ventricular ischemia, amelioration of which was attempted in this study using nitroglycerin. Hemodynamic variables were assessed during inflation of an angioplasty balloon in the proximal left anterior descending coronary artery of 10 patients. Regional wall motion was assessed by left ventriculography during a separate balloon inflation. Nitroglycerin (200 micrograms) was then administered intravenously, and hemodynamic and ventriculographic assessments during balloon inflations were repeated. Balloon inflation resulted in a marked increase in left ventricular end-diastolic pressure (from 9.2 +/- 2.1 to 19.4 +/- 2.9 mm Hg) and time constant of left ventricular relaxation (from 44.2 +/- 6.2 to 62.3 +/- 11.3 ms) and a decrease in distal coronary artery perfusion pressure (from 54 +/- 9 to 33.1 +/- 4 mm Hg). Time to onset of angina was 29 +/- 3 seconds and time to ST segment depression of 1 mm or greater was 30 +/- 3 seconds. Regional wall motion analysis 30 seconds after onset of balloon inflation revealed marked hypokinesia and akinesia in the anteroapical segments with graduated depression of inferior wall motion, greatest at the apex. After the administration of nitroglycerin, balloon inflation resulted in a smaller increase in end-diastolic pressure (from 5.0 +/- 2.7 to 8.3 +/- 2.6 mm Hg) and time constant (from 47.9 +/- 4.7 to 54.4 +/- 9.2 ms; both p less than 0.01 versus standard balloon inflation). Distal coronary artery pressure remained similar to standard balloon inflation (32 +/- 3 mm Hg) despite lower mean arterial pressure (89 +/- 5 mm Hg, p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration by nitroglycerin of left ventricular ischemia induced by percutaneous transluminal coronary angioplasty: assessment by hemodynamic variables and left ventriculography. 316 Jul 55

The effect of several kinds of antianginal drugs: nitrates, coronary vasodilators, beta-adrenergic blocking agents and calcium entry blocking agents on the myocardial metabolism and myocardial acidosis during ischemia was studied in the dog heart in vivo. Ischemia was induced by ligating the left anterior descending coronary artery. Ischemia accelerated anaerobic metabolism in the myocardium, in which glycogen breakdown, accumulation of glycolytic intermediates, loss of high energy phosphate and tissue acidosis occurred. Nitroglycerin, beta-adrenergic blocking agents such as propranolol, and some calcium entry blocking agents such as diltiazem and flunarizine prevented the myocardial metabolism from shifting to an anaerobic metabolism in spite of ischemia. However, coronary vasodilators and the dihydropyridine type of calcium entry blocking agents were not capable of reducing changes in the myocardial metabolism and myocardial acidosis during ischemia. The author makes a point in the present review that all the drugs which dilate coronary artery are not always effective on the ischemic myocardium.
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PMID:[Ischemic myocardial metabolism and antianginal drugs]. 354 84

The paper presents an overview of the recent diagnostic and therapeutic feasibilities in acute coronary heart disease. In unstable angina the leading symptoms are new onset or increasing anginal pain or resting pain as well as ST-T-changes in the ecg without a rise in enzymes. Coronary arteriography shows double or triple vessel disease (70%), a left main stenosis (10 to 15%) or normal coronary arteries (10 to 15%). The treatment of unstable angina in the CCU consists of Nitroglycerin-infusion together with calcium channel blockers and/or betablockers. With this regimen, 80% of patients may be stabilized within 24 to 48 hours. Thereafter coronary arteriography is performed to settle the further therapeutic regimen (PTCA, CABG, medical therapy). Acute myocardial infarction is characterized by persisting (more than 30 min) pain, ST-T-changes in the ecg with or without development of Q-waves indicating irreversible myocardial damage. Angiographically, usually a subtotal or total occlusion of the corresponding artery is found. Aims of therapy in acute myocardial infarction is-besides treatment of complications like arrhythmias and left ventricular failure-reperfusion of the myocardium with reopening of the occluded vessels by intracoronary or systemic thrombolysis. Recently, also clot-specific streptokinase derivates and plasminogen activators are used with fewer bleeding complications. After recanalization of the vessel a persisting stenosis should be relieved either by PTCA or CABG to avoid reocclusion. However, these active forms of treatment can only be performed, if the patient reaches the hospital within 4 to 6 hours after the onset of ischemia.
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PMID:[Acute coronary heart disease. Current status of diagnostic and therapeutic possibilities in the intensive care station]. 372 2

The treatment of postoperative hypertension with nitroglycerin or nitroprusside reduces cardiac filling, and volume loading is required to maintain hemodynamic and metabolic stability. Postoperative hypertension (mean arterial pressure greater than 95 mm Hg) developed in 33 patients who were randomized to an initial infusion of nitroglycerin or nitroprusside in a crossover trial. Volume loading (a rapid infusion of 250 to 500 ml of colloid to raise the left atrial pressure 2 to 4 mm Hg) was instituted prior to hypertension and again following the crossover trial during the infusion of nitroglycerin (11 patients) and nitroprusside (13 patients). Volume loading increased left ventricular end-diastolic volume index (LVEDVI) as documented by nuclear ventriculography, cardiac index (CI), and left ventricular stroke work index (LVSWI). Although CI was higher (p less than 0.01) with nitroprusside at any level of LVEDVI, myocardial performance (the relation between LVSWI and LVEDVI) was not different. Diastolic compliance (the relation between left atrial pressure and LVEDVI) was increased (p less than 0.01) with nitroglycerin. Myocardial metabolism was assessed by calculating myocardial lactate flux (MVL), the product of myocardial lactate extraction and coronary sinus blood flow by the thermodilution technique. Volume loading increased MVL during nitroglycerin therapy and decreased (p less than 0.01) MVL during nitroprusside therapy. Volume loading restored preload and increased CI with both nitroglycerin and nitroprusside. Only nitroglycerin improved myocardial lactate utilization. Nitroglycerin is the preferred vasodilator when ischemia is suspected after coronary bypass operations.
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PMID:A comparison of nitroglycerin and nitroprusside: II. The effects of volume loading. 391 60

Nitroglycerin plaster (in 5 cm2, 10 cm2 or 20 cm2 sizes) was applied to 12 patients with coronary heart disease, angina and exercise-induced ischemic reactions in the course of a simple-blind trial with intra-individual crossover in a randomized sequence over one week each. A 15 cm2 plaster served as a placebo. In the placebo phase the mean number of angina attacks was 9.3 per week. It decreased to 6.2 with the 10 cm2 plaster (P less than 0.05), to 2.6 per week with the 20 cm2 plaster (P less than 0.001). The ischemia reaction in the exercise ECG (sum of ST segment depressions), recorded on day 7 of the treatment phase, was improved three hours after plaster application, dependent on the size of the plaster: placebo 6.0 +/- 1.2 mm; 5 cm2 plaster 5.1 +/- 1.0 mm; 10 cm2 4.6 +/- 1.0 mm (P less than 0.05); 20 cm2 3.4 +/- 0.9 mm (P less than 0.001). The angina-free period during ergometry showed dose-dependent improvement 3 and 24 hours after application. Arterial blood pressure was decreased only after 20 cm2 plaster by 8% after three hours, as compared with the placebo (P less than 0.05). There was no effect on heart rate, at rest or on exercise, after any plaster. The results indicate that significant decrease in ischemia reaction occurred with a plaster of 10 cm2 or larger. A 24-hour effect was demonstrable only with respect to the duration of symptom-free exercise.
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PMID:[Anti-anginal effect of transdermally applied nitroglycerin as dependent on the size of the plaster]. 391

Nitroglycerin (NTG) and isosorbide dinitrate (ISDN) are potent dilators of vascular smooth muscle. The organic nitrates produce venodilation at very low doses, with little additional vasodilation of the venous circulation with increasing dosage. Nitrates increase arterial diameter and improve arterial conductance at low to moderate doses, and at high doses these agents produce dilation of the arteriolar or resistance vessels of the body. The overall hemodynamic response to nitrate administration will be modulated by the degree of sympathetic reflex discharge, the presence or absence of congestive heart failure, the dosage of administered nitrate, and the presence or absence of nitrate tolerance. Regional circulatory effects of the organic nitrates include a decrease in vascular resistance and an increase in arterial blood flow to the arms and legs. Venodilation also occurs in the extremities. In the splanchnic and mesenteric circulations, nitrates induce an initial vasodilative response followed by reflex vasoconstriction. Hepatic blood flow changes little in the normal state. Pulmonary blood flow decreases and pulmonary artery and venous pressures fall after nitrate administration. Renal blood flow remains essentially unchanged or decreases slightly after NTG administration, although reflex sympathetic activity may cause secondary vasoconstriction. The antianginal effects of nitrates have long been thought to be related to their systemic or peripheral actions, which reduce myocardial oxygen requirements through decreases in left ventricular preload and afterload. There is, however, considerable evidence that nitrates have important direct effects on the coronary circulation in both the normal and the ischemic heart. Such actions include coronary artery dilation, increased collateral blood flow, and enhanced oxygenation and nutrient perfusion to zones of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of nitroglycerin and long-acting nitrates. 392 41

Nitroglycerin and other organic nitrates exert a number of favorable effects on the circulation of patients with severe congestive heart failure, and these effects mediate the short- and long-term hemodynamic and clinical improvement that follows treatment with these drugs. Although these agents are potent dilators of systemic venous capacitance vessels, present evidence indicates that they do not exert their beneficial hemodynamic and clinical effects by decreasing venous return to the heart. Rather, their ability to dilate pulmonary and systemic resistance vessels offsets any decrease in cardiac output that might be expected to occur from a decrease in venous return. Of equal importance, the increase in output of the left side of the heart that results from drug-induced pulmonary and systemic vasodilation prevents any decrease in venous return to the right side of the heart that might be expected to accompany an increase in systemic venous capacitance. The net effect of these two interacting forces is not only to keep cardiac output and venous return constant but also to translocate blood volume from the pulmonary circulation and left ventricle to the systemic vessels. In addition, nitrates also relieve subendocardial ischemia and favorably alter pressure-volume relationships in the left ventricle. These observations support the conclusion that the complex cardiovascular responses to organic nitrates in patients with congestive heart failure cannot be adequately summarized by the single concept of preload reduction.
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PMID:Mechanisms of nitrate action in patients with severe left ventricular failure: conceptual problems with the theory of venosequestration. 392 45

Nitroglycerin (TNG) causes a prolonged dilatation of coronary collaterals. To demonstrate a functional significance of this dilatation we measured the effect of TNG on myocardial contractile force in dogs 2(1/2)-4 wk after the left anterior descending coronary artery (LAD) had been embolized in closed-chest animals. Development of collaterals was documented by angiography. Via a left thoracotomy the main left coronary artery (LCA) and LAD distal to the embolized plug were cannulated. Coronary flow and perfusion pressure were recorded. Contractile force was measured with gauges sutured to epicardial areas supplied by the left circumflex coronary artery (LCf) and occluded LAD. Coronary perfusion pressure in the LCA was gradually decreased until the contractile force recorded by the LAD gauge diminished while the LCf gauge was unaffected. Under these conditions, with coronary perfusion pressure held constant with the aid of a Starling resistance, TNG (18 mug) injected into the LCA increased peripheral LAD pressure by 3-12 mm Hg and contractile force in the LAD region by 36% (range 20-90%), returning it to near-normal levels, while having minimal effect in the LCf area. These changes persisted for 5 min. When LCf and LAD areas were both ischemic, intracoronary TNG had minimal effect on peripheral LAD pressure and contractile force. Thus, TNG causes prolonged dilatation of coronary collaterals and presumed increased collateral flow with subsequent enhancement of myocardial contractile force in ischemic areas. This effect is seen only when ischemia is limited to an area supplied by the collaterals. When the whole heart is ischemic, collaterals are unresponsive to TNG, suggesting that these collaterals dilate fully when the regions from which they originate become ischemic.
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PMID:The effects of nitroglycerin on coronary collaterals and myocardial contractility. 420 Dec 67

The effect of intracoronary administration of nitroglycerin on the distribution of cardioplegia and myocardial cooling was assessed in 45 patients undergoing elective myocardial revascularization. The patients were divided into three groups. Myocardial temperature was measured over the right and left coronary artery distributions in Group 1 after the infusion of 1 liter of potassium blood cardioplegic solution (20 mEq of potassium per liter). Similar temperature measurements were made in Group 2 after the addition of 300 micrograms of nitroglycerin to the cardioplegic solution and in Group 3 after the addition of 1,000 micrograms of nitroglycerin. Nitroglycerin did not affect myocardial cooling, and large temperature gradients persisted after delivery of cardioplegia in patients with occlusive coronary artery disease. Unexpectedly, however, the rate of cardioplegia delivery increased by 134%, within the same range of infusion pressures, in patients receiving nitroglycerin. Although nitroglycerin cardioplegia does not affect the regional disparity in the distribution of cardioplegia in patients with severe coronary artery disease, intracoronary administration of nitroglycerin reduces the time required for administration of cardioplegia and thereby decreases the total ischemia time.
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PMID:The effect of nitroglycerin cardioplegia on myocardial cooling in patients undergoing myocardial revascularization. 640 12

Nitroglycerin and nitrates have long been contraindicated in the treatment of acute myocardial infarction. Beneficial effects, however, are reported in patients with left ventricular failure. In this report the available data from the literature are reviewed with respect to the influence of the drug on myocardial ischemia, infarct size and necrosis as well as on ventricular arrhythmias and prognosis. All authors have confirmed a beneficial influence of nitroglycerin on myocardial ischemia and QRS signs of necrosis. Some authors have demonstrated a reduction in CK and CKMB activity. Ischemia-related ventricular dysrhythmias were also effectively reduced. Some promising data are available on prognosis.
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PMID:Nitroglycerin therapy in acute myocardial infarction--an overview. 642 Oct 5


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