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)

The rationale for using intravenous nitrates in patients hospitalized with severe angina pectoris is that physiologic action is almost immediate. Many studies and clinical experience indicate that the use of this preparation results in a marked diminution of recurrent angina episodes in most patients. If adverse reactions such as severe hypotension or bradycardia occur, decreasing the dose or stopping it entirely corrects the problem. Intravenous nitroglycerin can be used in combination with other known antianginal agents, such as beta blockers and calcium antagonists. In clinical practice most patients are treated with nitrates and beta blockers or calcium antagonists because the combination of drugs may reduce ischemia and symptoms more than each drug used alone over a long period.
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PMID:Use of nitrates in unstable angina pectoris. 289 Dec 89

Recent studies show that in many coronary artery disease patients with any form of angina, myocardial infarction, or positive exercise tests but no symptoms, most of the ischemic episodes are silent. Furthermore, evidence is building to suggest that in many patient groups, silent ischemia relates to prognosis. Numerous therapies, including nitroglycerin or isosorbide dinitrate, have been shown to modify silent ischemia and its associated risks. Studies indicate that frequency and perhaps duration of silent ischemic episodes can be modified by treatment with beta-adrenergic blockers or calcium antagonists alone or, even more effectively, with a combination of both types of agent. Many ischemic episodes persist, however, when therapy is directed only at reduction of angina. Evidence suggests that some characteristics of silent ischemia predict prognosis, whereas angina characteristics do not. Until additional data about prognosis and the influence of treatment on prognosis are available, the appropriate focus seems to be improvement of outcome in those patients who are at highest risk, rather than only reduction of chest pain.
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PMID:Silent myocardial ischemia. Rationale for management. 289 63

Episodes of myocardial ischemia in patients with coronary artery disease may be due to transient increases in coronary vasomotor tone superimposed on a fixed atherosclerotic obstruction. The purpose of this study was to determine whether identification of the clinical pattern of angina could predict the therapeutic response to the addition of nifedipine to a regimen of beta blockers and/or long-acting nitrates. Seventy-two patients with stable exertional angina were divided into two groups: "classic exertional angina" (17 patients), defined as exertional angina with a stable threshold; and "mixed angina" (55 patients), defined as exertional angina provoked by a variable threshold and/or at least two episodes of rest angina within the 3 months prior to screening. Patients were studied with nifedipine and placebo in a 6-week, double-blind, crossover design that used serial anginal diaries, exercise treadmill tests, and 24-hour ambulatory ECG monitoring. In patients with mixed angina, nifedipine reduced the frequency of angina compared to that during placebo treatment (13.1 vs 9.9 episodes/3 weeks, p less than 0.01) and reduced nitroglycerin consumption (11.7 vs 7.5 tablets/3 weeks, p less than 0.05); while in patients with classic exertional angina, nifedipine had no symptomatic effect (7.9 vs 6.8 anginal episodes/3 weeks, NS; 6.4 vs 5.8 nitroglycerin tablets/3 weeks, NS). Patients in both groups experienced a significant decrease in the manifestations of ischemia during exercise testing. Patients with mixed angina experienced a reduction in the daily frequency of painful episodes of ST segment depression during nifedipine treatment compared to placebo (0.6 vs 0.2 episodes, p less than 0.05), but there was no effect on the frequency of episodes of silent ischemia (4.2 vs 3.4 episodes, NS). In patients with classic exertional angina, the addition of nifedipine had no effect on any measure of ambulatory ischemia. We conclude that patients with mixed angina are more likely to benefit symptomatically from the addition of nifedipine therapy than patients with classic exertional angina. The lack of a consistently preferential response to nifedipine in patients with mixed angina, however, suggests that episodic coronary vasoconstriction may not be the only mechanism responsible for ischemia in these patients, and/or that nifedipine may not necessarily provide additional therapeutic benefit beyond that conferred by a regimen of beta blockers and/or nitrates.
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PMID:The efficacy of the addition of nifedipine in patients with mixed angina compared to patients with classic exertional angina: a multicenter, randomized, double-blind, placebo-controlled clinical trial. 290 79

Coronary artery spasm unresponsive to intracoronary nitroglycerin was observed in eight patients undergoing percutaneous transluminal coronary angioplasty for unstable ischemic symptoms (unstable angina or recent nontransmural infarction, or both). All patients manifested eccentric lesions angiographically with the right coronary artery involved in four, circumflex artery in two and left anterior descending in two. Severe coronary spasm was documented angiographically in all patients after angioplasty and resulted in symptomatic and electrocardiographic evidence of ischemia. Multiple sites of spasm were present in the dilated vessel in three patients. Coronary artery spasm persisted despite the infusion of large doses of intracoronary nitroglycerin (200 to 2,000 micrograms, mean 850 micrograms) over 10 min. Administration of intracoronary verapamil (1 to 1.5 mg over 10 min) resulted in complete relief of spasm with restoration of brisk anterograde flow in all patients. These findings suggest that intracoronary verapamil may be a useful agent for the relief of coronary spasm occurring in the setting of coronary angioplasty.
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PMID:Intracoronary verapamil for reversal of refractory coronary vasospasm during percutaneous transluminal coronary angioplasty. 297 6

Early experience with the use of tissue plasminogen activator (tPA) in acute myocardial infarction is reviewed, including comparisons with other thrombolytic agents, a summary of hemorrhagic complications associated with its use, and the rationale for adjunctive therapeutic strategies. The use of tPA has been associated with improvement in left ventricular function, a lower mortality, and a decrease in congestive heart failure signs and symptoms. A protocol for evaluation of patients with possible myocardial infarction for thrombolytic therapy is presented. Consideration must be given to other possible diagnoses, and the ECG must be evaluated carefully to ensure that appropriate criteria are met. Risk factors for hemorrhagic complications include recent trauma, surgery, gastrointestinal and genitourinary bleeding, stroke, and focal neurologic findings. Greater benefit of therapy is expected in patients with larger infarcts who have more marked ST segment changes or evidence of hemodynamic compromise, especially when they are treated early after the onset of symptoms (within the first several hours). Adjunctive measures that can be considered in the emergency department include prophylactic lidocaine, IV nitroglycerin, beta blockade, aspirin, volume replacement and monitoring for dysrhythmias, bleeding, and recurrent ischemia. A comprehensive understanding of these rapidly evolving concepts will assist the emergency physician in the evaluation and management of patients with acute myocardial infarction.
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PMID:Experience with the use of tPA in the treatment of acute myocardial infarction. 297 70

In distant heart procurement, optimal storage conditions remain to be defined, especially with respect to the electrolytic concentrations of storage solutions. Between December 1986 and April 1987, heart transplants were carried out in 18 patients. After cardioplegic arrest (St. Thomas), the hearts were randomly stored in either Euro-Collins' solution (ECS; n = 9) or Ringer's solution (RS; n = 9) at 4 degrees C. For the first 24 h postsurgery, atrial pressures (LAP, RAP), systemic (MAP) and pulmonary pressures (PAP), and cardiac output (CO) were monitored. In addition, catecholamine and nitroglycerin requirements as well as the type of cardiac rhythm were documented. There was no significant difference between the groups in terms of the period of graft ischemia (ECS, 162 +/- 28 min; RS, 141 +/- 47 min); the MAP, RAP, LAP, and CO were also similar in both groups. The total amount of epinephrine needed to maintain the MAP between 60 and 80 mm Hg was 10.5 mg/24 h +/- 4.1 mg in ECS compared with 19.9 mg/24 h +/- 12 mg in RS (P less than 0.05). Despite less inotropic support, the left cardiac work index was considerably higher in the ECS group (P less than 0.05). In the first few postoperative hours, 8/9 RS patients needed either atrial (n = 4) or ventricular pacing (n = 4) for a heart rate of 90-100 beats/min (bpm), whereas only three ECS patients required atrial pacing (P less than 0.05). All other ECS hearts showed a spontaneous sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distant heart procurement. Impacts of storage solution composition on cardiac performance following transplantation. 307 73

The efficacy of PY 108-068 (75 and 150 mg/day), a new dihydropyridine calcium antagonist, was compared with placebo for treatment of chronic stable angina. Twelve patients were studied in a placebo-controlled, double-blind, randomized, crossover trial of 2 weeks each. Antianginal efficacy was assessed by the number of episodes of angina and nitroglycerin tablets consumed during each 2-week period, as well as the number of episodes of ischemia during 48-hour ambulatory monitoring and the area and severity of ST-segment depression during 16-point precordial exercise mapping. Nitroglycerin consumption (mean +/- standard error of the mean) decreased from 6.1 +/- 2.9 with placebo to 1.8 +/- 1.5 with 75 mg/day of PY 108-068 (p less than or equal to 0.03) and to 3.6 +/- 2.3 with 150 mg/day of PY 108-068 (p less than or equal to 0.01 vs placebo, difference not significant vs 75 mg/day of PY 108-068), whereas episodes of angina were reduced significantly only by the high dose (p less than or equal to 0.03) (11.1 +/- 3.9 with placebo, 6.3 +/- 2.4 with 75 mg/day of PY 108-068 and 8.1 +/- 3.4 with 150 mg/day of PY 108-068). The low dose alone significantly reduced ST-segment depression during exercise testing (p less than or equal to 0.03) (29.6 +/- 3.6 with placebo, 23.1 +/- 5.6 with 75 mg/day of PY 108-068 and 24.4 +/- 5.0 with 150 mg/day of PY 108-068), whereas neither dose significantly altered the number of episodes of ischemia during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of PY 108-068, a new calcium channel blocker, for angina pectoris. 307 40

Coronary microvascular damage appears to play a role in reperfusion injury after myocardial ischemia. This study was designed to afford direct viewing of the effects of myocardial ischemia-reperfusion on the coronary microcirculation and to determine whether pretreatment with the calcium blocker nisoldipine would attenuate any microvascular damage during reperfusion. Four groups of isolated rat hearts were perfused with a solution that contained red cells and fluorescent albumin, but was essentially free of platelets and leukocytes. Group I served as a nonischemic control. Group II hearts were subjected to 30 minutes of no-flow ischemia followed by reperfusion. Group III hearts were pretreated with nisoldipine (1 microgram/min) for 5 minutes before ischemia, and group IV hearts were treated with nitroglycerin (93 micrograms/min) before and after ischemia to mimic the vasodilation caused by nisoldipine. Perfused coronary capillarity and transcoronary extravasation of plasma albumin were measured by direct visualization techniques before and after ischemia. For group I, there was no significant change in coronary resistance, perfused capillarity, or transcoronary extravasation with time. For both groups II and IV, ischemia-reperfusion caused no increase in coronary resistance, but a significant decrease in perfused capillarity and a marked increase in transcoronary extravasation of fluorescent albumin (P less than 0.05). The nisoldipine group (group III) demonstrated a similar decrease in perfused capillarity but no increase in protein extravasation during reperfusion. These results indicate that, in the heart, platelets and/or leukocytes are not absolutely necessary to induce either the no-reflow phenomenon or the permeability damage observed during reperfusion after ischemia. The protective effect of treatment with nisoldipine appeared to be independent of vasodilation. We speculate that this calcium blocker reduced endothelial uptake of calcium during reperfusion, preventing endothelial deformation and formation of interendothelial gaps.
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PMID:Prevention of transcoronary macromolecular leakage after ischemia-reperfusion by the calcium entry blocker nisoldipine. Direct observations in isolated rat hearts. 308 Feb 59

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise. 308 64

The effects of prophylactic infusion of 1 microgram X kg-1 X min-1 nitroglycerin (NTG) on the incidence of ischemia, hypertension, hypotension and perioperative myocardial infarction were studied in 81 patients during coronary artery bypass grafting (CABG). Forty-one patients (Group 1) received NTG and 40 patients (Group 2) received placebo. All patients received fentanyl for anesthesia and pancuronium. Mean arterial pressure (MAP), pulmonary capillary wedge pressure (PCWP), heart rate (HR), and cardiac output (CO) were measured before and after induction of anesthesia, after intubation, before and after chest incision, after sternotomy, after the pericardium was opened, and during normothermic cardiopulmonary bypass. Myocardial ischemia and infarction were diagnosed from the ECG, hypertension was defined as a 20% increase in MAP, and hypotension was defined as a 20% decrease in MAP compared with preinduction values. No significant differences between Groups 1 and 2 in HR, PCWP, or CO were seen. MAP was significantly lower in Group 1 than Group 2 (P less than 0.05) before chest incision, but increased to levels equal to Group 2 after sternotomy. Hypertension occurred in 32 Group 2 patients and 25 Group 1 patients (0.05 less than P less than 0.1). Group 1 patients had 0.95 +/- 0.14 episodes per patient of hypertension, while Group 2 patients had 2.10 +/- 0.31 episodes (P less than 0.05). Hypotension occurred in 20 Group 1 patients but only six Group 2 patients (P less than 0.05). There was no difference in the incidence of ischemia. In Group 1, nine patients (22%) had ECG changes of ischemia, while 12 patients in Group 2 (30%) had ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prophylactic nitroglycerin infusions during coronary artery bypass surgery. 308 41


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