Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

By the mid 1960s a beneficial effect of post-myocardial infarction treatment with beta-blockade had been proposed. However, it was not until 1981 that large clinical trials clearly demonstrated a beneficial effect both in terms of reduction in mortality and morbidity. Today treatment with beta-blockers both in the acute phase of acute myocardial infarction as well as in the stable post-myocardial infarction patient is well established. In this review article, different aspects of early and late treatment with beta-adrenoceptor blockers are discussed. The cardioprotective effects of beta-blockers on mortality and morbidity should not be considered class effects valid for all beta-blockers. Pooled data have clearly demonstrated that beta-blockers with intrinsic sympathomimetic activity have less marked effects. Impressive effects on mortality and morbidity have been obtained with propranolol, timolol, and metoprolol, which are noncardioselective as well as more beta 1-selective (metoprolol), but they are all lacking intrinsic sympathomimetic activity and, furthermore, have a relatively high degree of lipophilicity. It is clear that acute beta-adrenoceptor blockade in suspected acute myocardial infarction reduces mortality and morbidity as well as complications such as chest pain and ventricular arrhythmias during the acute phase. In post-myocardial infarction treatment, it is clear that both mortality and morbidity are reduced. Reports from extended follow-ups after termination of initial double-blind beta-blocker studies in postinfarction patients indicate that withdrawal of the active treatment may increase mortality after cessation of treatment. This is observed despite measures having been taken to avoid so-called acute withdrawal phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial infarction. Effects of beta-blockade. 168 4

Although beta-sympathomimetic tocolytic therapy has been associated with transient subendocardial ischemia, magnesium sulfate has rarely been noted to cause acute chest pain and is, in fact, known to improve myocardial perfusion in patients with variant angina. We believe this report represents the first case in which intravenous magnesium sulfate administered as a tocolytic agent caused acute chest pain accompanied by transient electrocardiographic evidence of subendocardial ischemia.
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PMID:Transient symptomatic subendocardial ischemia during intravenous magnesium sulfate tocolytic therapy. 173 14

A 28 yr-old male presented with chest pain and acute ST elevation following ingestion of pseudoephedrine. The pain and electrocardiographic changes disappeared after the administration of sublingual Nitroglycerin. Myocardial enzymes did show some evidence for myocardial necrosis. A subsequent coronary arteriogram showed no occlusive lesions. Pseudoephedrine, a sympathomimetic agent, may be implicated in the initiation of coronary spasm and myocardial infarction in some patients.
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PMID:Coronary artery spasm and myocardial infarction in a patient with normal coronary arteries: temporal relationship to pseudoephedrine ingestion. 234 9

Coronary heart disease is the most common cause of death in many Westernized countries. Patients who experience either a threatened myocardial infarction (MI) or an acute MI within the last 12 h or so can benefit from interventions that decrease myocardial oxygen demand. Beta-Blockade fulfills such a purpose mainly through diminishing the product of heart rate x systolic blood pressure. Added benefits of beta-blockade include (a) a redistribution of myocardial blood supply in favour of ischaemic areas, (b) inhibition of catecholamine-induced myocardial necrosis, and (c) a decrease in the Q-Tc interval and an increase in the threshold to ventricular fibrillation. Beta 1-Selective blockade is the essential ingredient; the possession of intrinsic sympathomimetic activity (ISA) may diminish benefit. Intravenous, followed by oral, beta-blockade within 12 h (preferably 6 h) of the onset of chest pain results in (a) a marked reduction in chest pain, (b) a reduction in infarct size by about 30%, (c) a diminished likelihood of threatened infarction progressing to overt infarction, (d) a reduction in the number of life-threatening ventricular arrhythmias, and (e) a reduction in the incidence of cardiac arrest and reinfarction. Intravenous, followed by oral, beta 1-selective blockade (atenolol) significantly reduces vascular mortality by about 15% at 1 week post-MI, and the benefit is maintained at 1 year. Such an intervention, provided contraindications to beta-blockade are respected, is safe and well tolerated. Probably about 50% of patients are eligible for such treatment. Such an approach is highly cost effective.
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PMID:Beta-blockade in acute myocardial infarction. 246 37

Flestolol (ACC-9089) is a nonselective, competitive, ultra-short-acting beta-adrenergic blocking agent, without any intrinsic sympathomimetic activity. Flestolol is metabolized by plasma esterases and has an elimination half-life of approximately 6.5 minutes. This agent was well tolerated in healthy volunteers at doses up to 100 micrograms/kg/min. In long-term infusion studies, flestolol was well tolerated at the effective beta-blocking dose (5 micrograms/kg/min) for up to seven days. Flestolol blood concentrations increased linearly with increasing dose and good correlation exists between blood concentrations of flestolol and beta-adrenergic blockade. Flestolol produced a dose-dependent attenuation of isoproterenol-induced tachycardia. Electrophysiologic and hemodynamic effects of flestolol are similar to those of other beta blockers. In contrast with other beta blockers, flestolol-induced effects reverse rapidly (within 30 minutes) following discontinuation because of its short half-life. Flestolol effectively reduced heart rate in patients with supraventricular tachyarrhythmia. In patients with unstable angina, flestolol infusion was found to be safe and effective in controlling chest pain. It is concluded that flestolol is a potent, well-tolerated, ultra-short-acting beta-adrenergic blocking agent. Use of flestolol in the critical care setting is currently undergoing investigation.
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PMID:Flestolol: an ultra-short-acting beta-adrenergic blocking agent. 287 85

24-hour ambulatory monitoring of the ST segment in patients with angina has shown that ST segment depression may be accompanied by angina pectoris, but it occurs equally often without any symptoms. Approximately half of all episodes of ST segment depression are accompanied by chest pain. Doubt has been expressed as to the significance of ST segment changes that occur in the absence of chest pain, but haemodynamic studies and nuclear imaging have shown that such changes are accompanied by alterations in left ventricular filling pressure. Ambulatory pulmonary artery monitoring has also shown that silent ST segment depression is accompanied by a significant increase in pulmonary artery diastolic pressure, and this does not differ from painful episodes of ST segment depression. Studies using ambulatory monitoring have shown that antianginal drugs are capable of reducing the frequency of ST segment depression accompanied by pain. We have recently performed studies investigating the use of antianginal medications; i.e. beta-blocking drugs with and without sympathomimetic activity, alpha-beta-blocking drugs, calcium antagonists and nitrates in the treatment of both painful and painless ST segment depression. These studies have shown that the effect of these drugs on painless episodes is similar to their effect on painful episodes of myocardial ischaemia. Although the prognostic implications of silent ischaemia and the importance of these therapeutic findings are unknown, it is well known that approximately one-quarter of all myocardial infarctions occur without chest pain. Moreover, recent investigations in unstable angina show that silent myocardial ischaemia is an important predictor of future coronary events.
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PMID:Should we treat silent ischaemic? 362 15

The medical complications of cocaine abuse are being encountered by clinicians with increasing frequency. The cardiovascular manifestations of cocaine abuse include chest pain, myocardial ischemia and infarction, congestive heart failure, arrhythmias, infective endocarditis, and aortic dissection. The pathogenesis of these cardiovascular complications has not been fully elucidated but may be related to a combination of the sympathomimetic and membrane anaesthetic effects of cocaine. We present these concepts in a case discussion format.
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PMID:Cardiovascular manifestations of cocaine abuse. A case of recurrent dilated cardiomyopathy. 777 43

Cardiovascular problems are among the most frequently seen medical complaints related to cocaine use, with chest pain as the most commonly encountered cardiac emergency. Multiple studies and case reports have documented myocardial infarction in young, otherwise low-risk cocaine users. Treatment should be consistent with that of any patient with myocardial ischemia, with particular attention devoted to decreasing the sympathomimetic effects of the cocaine. A 24-hour observation period identifies close to 100% of patients sustaining an acute myocardial infarction after cocaine use.
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PMID:Cocaine chest pain. 818 89

A 48-year-old man with a history of hypertension and diabetes mellitus was hospitalized with sudden onset of severe chest pain. He was in cardiogenic shock with a systolic pressure of 60 mm Hg. His electrocardiogram (ECG) showed ST-segment elevation in the precordial leads suggestive of acute anteroseptal myocardial infarction. The ST-segment returned to baseline after the systolic blood pressure rose to 100 mm Hg with the administration of sympathomimetic agents. Aortography and transesophageal echocardiography demonstrated type A aortic dissection and aortic regurgitation. Aortography and short-axis transesophageal echocardiography showed during diastole almost complete collapse of the true lumen of the ascending aorta caused by the intimal flap. The patient underwent surgical repair of the aortic dissection and implantation of Palmaz stents in the carotid arteries. Decreased blood pressure and the presence of aortic regurgitation accelerated the collapse of the true lumen during diastole in the ascending aorta, resulting in functional obstruction of the left main coronary artery, which may have been related to ST-segment changes in this case.
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PMID:A case of aortic dissection with transient ST-segment elevation due to functional left main coronary artery obstruction. 1071 27


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