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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The haemodynamic effects of a new beta-adrenergic blocking agent KO.1366 (bunitrolol) were assessed in 10 males admitted to hospital for investigation of chest pain. Measurements were made at rest, during atrial pacing at 100 beats/min, and during hand grip exercise, before and afterintravenous administration of KO.1366 at a dosage of 0.05 mg/kg body weight. There was a 12% (p less than 0.01) slowing in resting heart rate and alpha 4% (p less than 0.05) slowing in exercise heart rate after drug administration. Resting left ventricular end diastolic pressure rose by 2.2 mm Hg (p less than 0.01) following the drug, but there was no significant change during pacing or exercise. Left ventricular systolic pressure and its first derivative did not change significantly. Cardiac output rose slightly, and stroke volume at rest and during exercise showed a considerable increase. In the dosage used, KO.1366 has an important chronotropic effect on the heart without causing significant myocardial depression.
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PMID:Haemodynamic observations with KO. 1366 (bunitrolol), a new beta-adrenergic blocking agent. 2 26

Prinzmetal's variant of angina occurred in a 48-year-old man who sustained two attacks of subarachnoid hemorrhage within 10 days. The first anginal pain started at the same time that the second cerebrovascular accident developed, but subsequent anginal episodes were not accompanied by other symptoms or signs that indicated new development of subarachnoid hemorrhage. Twelve days later, when nuchal rigidity was fairly improved, the episodes of chest pain ended. A vasospasm of the large coronary arteries--probably due to the derangement of the autonomic nervous system caused by subarachnoid hemorrhage--was presumed to contribute to the occurrence of the variant angina. Based on this case and on review of the literature, we propose that coronary arterial spasm is one of several causes of the cardiac changes seen in subarachnoid hemorrhage.
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PMID:Prinzmetal's variant angina associated with subarachnoid hemorrhage: A case report. 43 81

Cardiac muscle death caused by coronary artery occlusion is a dynamic process that often takes hours or days. Emergency revascularization (saphenous vein bypass graft (SVBG) during acute myocardial infarction (MI) can interrupt myocardial necrosis, salvage ischemic myocardium and revascularize vessels with obstructive lesions not involved in the MI. In this report we describe a preliminary experimental study of 75 patients in which emergency SVBG was the therapy for acute MI. Group 1, 16 patients, required vasoactive medications and/or intraaortic balloon pumping to maintain their blood pressure preoperatively. There was one operative death and two late deaths. Group 2 consisted of 59 hemodynamically stable patients. There were no deaths. The average preop CPK in group 1 was 892 vs 504 in group 2 (p greater than 0.05). Surgical techniques were routine. The average time from the onset of chest pain that continued to surgery was 6.5 hours. Forty patients were restudied. Post- vs presurgical hemodynamics revealed ejection fraction increased by 34% (p greater than 0.05), left ventricular end-diastolic pressure reduced by 40% (p greater than 0.01). End-systolic and end-diastolic volume reduced by 30% (p greater than 0.05), and 15% (p greater than 0.01), and stroke volume improved 25% (p greater than 0.05). Operative mortality was 1.3% and late mortality 2.8%. These results suggest that cautious continued trial of emergency SVBG in patients with evolving MI is warranted.
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PMID:Emergency coronary artery revascularization: a possible therapy for acute myocardial infarction. 44 42

The technique for measuring platelet aggregate ratios described by Wu and Hoak (1974) was evaluated in normal subjects. The following had no influence upon the test result: age, sex, fasting versu the postprandial state, and the degree of stasis prior to drawing the sample. Variance within subjects was small compared to variance between subjects (0.009 versus 0.0053, p less than 0.01). Platelet aggregate ratios were then measured in 36 patients with coronary artery disease hospitalized with acute chest pain. Their mean platelet aggregate ratio of 0.86 was identical to the mean ratio for 47 normal subjects. Greater variability was found within patients (between samples) than within the normal subjects. This observation raises doubts about the significance of a single measurement of platelet aggregate ratio in such acutely ill patients. Mean platelet aggregate ratios measured daily did not differ over a 7-day period between 11 patients who developed a myocardial infarction and 10 patients who did not. A normal mean platelet ratio was also found on a single measurement from 30 patients with a history of completed stroke (0.87) and from 11 patients with a history of transient ischemic attacks (0.92).
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PMID:Platelet aggregate ratios--standardization of technique and test results in patients with myocardial ischemia and patients with cerebrovascular disease. 57 5

Hemodynamic changes were studied in ten patients with uncomplicated transmural myocardial infection during 24 hours on beta-blockade. The cardioselective beta-adrenergic blocking drug metoprolol was injected (15 mg i.v.) within the first 24 hours after onset of chest pain and was followed by oral therapy (25-50 mg at 6-hour intervals). There was a decrease in heart rate, systolic BP, and cardiac output, which was most marked after the injection. The stroke volume and diastolic BP for the whole group of patients remained unchanged. The pulmonary artery end diastolic pressure did not change significantly after the injection but a continuous fall was obtained in three out of four patients with initially elevated values. The preejection period, measured from the ECG and carotid pressure curve, as initially short and was prolonged in all patients after administration of the beta-blocking drug. It is concluded that the cardioselective beta-blocking drug metoprolol may be used in selected patients in the acute phase of myocardial infarction without danger of hemodynamic deterioration during the first 24 hours of therapy. The selection of patients can be based on clinical criteria. In this study signs of left heart failure, hypotension, poor peripheral circulation, bradycardia, and AV block were regarded as contraindications.
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PMID:Hemodynamic effects of the cardioselective beta-blocking agent metoprolol in acute myocardial infarction. A 24-hour catheterization study. 69 20

Fourteen patients with acute myocardial infarction were given 0.3 mg sublingual nitroglycerin within the first 12 hours of their acute myocardial infarction. Five minutes after sublingual nitroglycerin mean arterial pressure fell 9 mmHg (1.2 kPa) and remained significantly reduced for 30 minutes. Pulmonary capillary wedge pressure fell from a mean control value of 17 to 12 mmHg (2.3 to 1.6 kPa) and also remained reduced for 30 minutes. Heart rate was significantly raised and stroke work index reduced at five minutes. Patients with a stroke work index of greater than 55 g m per m-2 b.s.a. responed to nitroglycerin with a fall in both pulmonary capillary wedge pressue and strokework index while in those with a stroke work index of less than 55 g m per m-2 b.s.a. stroke work index did not fall concomitantly with the fall in pulmonary capillary wedge pressure. In one patient, nitroglycerin led to a precipitious fall in arterial pressure andrecurrence of chest pain.
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PMID:Role of sublingual nitroglycerin in patients with acute myocardial infarction. 80 10

Systolic time intervals and the a/H ratio were recorded in 20 patients with uncomplicated acute myocardial infarction over a period of five days. The initial high heart rate and systolic blood pressure and the short PEP and ICT indicating a sympathetic overactivity were spontaneously normalized during the first week of infarction. LVET was reduced indicating a fall in stroke volume and the a/H ratio was unchanged at the high levels suggestive of elevated preload or LVEDP. In 10 patients with acute myocardial infarction and recurrent chest pain recordings on noninvasive parameters were made before and 30 min after intravenous injection of practolol. In addition, 7 patients with chest pain, classified as acute myocardial infarction, were given practolol. The average dose of practolol was 17.9 mg ranging from 5 to 30 mg. An almost immediate and pronounced relief of pain was observed in all patients and no signs of impaired left ventricular function appeared. The product of systolic blood pressure and heart rate was decreased by practolol and the PEP and the ICT were prolonged to normal values while no changes were seen in LVET and a/H ratio. On 126 occasions practolol was given in dosages ranging from 5 to 30 mg (mean 8 mg) to 75 patients with acute myocardial infarction and recurrent chest pain. A satisfactory pain relief was seen on 108 occasions. It is suggested that an inappropriate sympathetic overactivity is an important factor in provoking recurrent chest pain in acute myocardial infarction. Administration of the beta-adrenergic blocking agent practolol resulted in pain relief due to reduction of heart work and in severity of myocardial ischemia. The beta-blocking agent was well tolerated in the present study. Continuous beta-blockade during the whole hospital stay to patients with acute myocardial infarction seems to be a very attractive therapy in order to preserve the ischemic myocardium and limit the size of infarction.
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PMID:Effect of cardioselective beta-blockade on heart function and chest pain in acute myocardial infarction. 106 28

Hemodynamic and metabolic responses to pacing from either the coronary sinus or right atrium were evaluated in 41 patients with chest pain and normal coronary arteriograms. A group of patients (group II) with angina, lactate production, or significant ST segment depression had a significantly higher mean pulmonary capillary pressure on peak pacing or angina than did a group of patients considered to have a normal pacing response (group I). In 6 of 9 group II patients, the left ventricular end-diastolic pressure either rose abnormally with pacing or was greater than 14 mm Hg immediately after pacing and resembled that of a group of patients with coronary artery disease; Patients with a prolapsing mitral valve (group III) also had a significantly higher pulmonary capillary pressure on peak pacing as compared to those of group I, although abnormal left ventricular pressure responses occurred in only 2 of 9 of these patients. The stroke index was significantly lower in group III on peak pacing while group II was no different from group I. Lactate production occurred in 6 of 9 group II patients. However, only 1 of 6 patients with a prolapsing mitral valve who were studied for lactate production was found to produce lactate, suggesting a different mechanism for their pain.
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PMID:Hemodynamic and metabolic responses to pacing in patients with chest pain and normal coronary arteriograms. 120 72

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.
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PMID:Beta-blockers: primary and secondary prevention. 128 45

Cicloprolol is a new beta-blocking agent with high selectivity for beta 1 receptors and high intrinsic sympathomimetic activity. We studied the acute hemodynamic effects of cicloprolol in nine subjects with no evidence of left ventricular dysfunction who underwent cardiac catheterization for the evaluation of chest pain. All patients had normal coronary angiography and left ventriculography. Left ventricular pressure was determined throughout the cardiac cycle using a Millar 8Fr Minotip catheter; an echocardiogram, phonocardiogram, and ECG were simultaneously recorded to obtain left ventricular pressure-diameter loops. All the measurements were repeated before and after the intravenous administration of cicloprolol. Cicloprolol was administered at increasing doses of 0.05, 0.10, and 0.25 mg/kg until a cardiac output increase of at least 15% over basal values was achieved. A decrease of mean arterial pressure or cardiac output after cicloprolol was not observed in any patient. Cicloprolol administration significantly increased cardiac output (24%), stroke volume (22%), and peak positive dP/dt (25%); no significant changes in heart rate, systemic blood pressure, right atrial pressure, or pulmonary artery pressures were observed. No significant change in the echocardiographic parameters occurred. Among the indices of left ventricular diastolic function, the time constant of isovolumetric relaxation was significantly decreased (-43%) after cicloprolol; moreover, the left ventricular pressure-diameter loop in the protodiastolic phase was shifted to the left following cicloprolol infusion. This study confirms that in subjects with normal left ventricular function cicloprolol can improve resting left ventricular systolic function, and it shows that this action can also be attended by a more rapid isovolumetric relaxation, similar to what has been observed with other sympathomimetic amines.
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PMID:Combined invasive and noninvasive study of left ventricular systolic and diastolic function following acute administration of cicloprolol to subjects with normal cardiac function. 136 Feb 56


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