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

To elucidate the relationship between heart rate (HR) and left ventricular ejection time (LVET) during early exercise, 30 patients with chest pain were studied at 1 (1') and 4 minutes (4'). Mean results for control leads to 1' exercise: HR 79 to 105 beats per minute, LVET 247 to 260 msec. Thus instead of shortening as predicted by the HR change at 1' of exercise, LVET rose significantly (p less than 0.001). Subsequently LVET fell as HR continued rising, and by 4' had fallen toward control level. This phenomenon is comparable to the paradoxical decline in LVET as HR decreases early post-exercise and is comparably explained by transiently disproportionate change in determinants of LVET, stroke volume, and ejection rate. Absence of difference in response of exercise-positive (ST depression greater than or equal to 1 mm) and exercise-negative patients, also supports this initial paradoxical lengthening in LVET as a physiologic response.
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PMID:Elucidation of physiologic lengthening of left ventricular ejection time during early upright exercise. 746 37

A 33-year-old man with heat exhaustion was admitted to our hospital suffering from severe chest pain. Serum creatine kinase elevation and new Q waves revealed myocardial infarction of the inferior wall. Technetium-99m-pyrophosphate suggested diffuse myocardial damage, although the left ventricular function was normal by echocardiography. This case highlights the importance of early recognition of heat stroke and heat exhaustion, as they are associated with widespread tissue injury.
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PMID:Acute myocardial infarction in a young man after heat exhaustion. 772 9

Dopexamine hydrochloride is a new synthetic catecholamine for intravenous use in low cardiac output states with co-existing raised systemic or pulmonary vascular resistance. Dopamine has been commonly used since several years in these situations. The drawbacks of dopamine include a vasoconstrictive effect with high infusion rates, and a marked tendency for ventricular ectopy due to the potent beta-1 adrenergic stimulation. Dopexamine hydrochloride has interesting vasodilator properties, with marked intrinsic agonist activity at beta-2 adrenoreceptors and a lesser agonist activity at dopaminergic receptors (DA1 and DA2). Its mild inotropic activity arises primarily from baroreceptor reflex stimulation with a possible contribution from direct stimulation of myocardial beta 2-adrenoreceptors. Dopexamine hydrochloride is responsible for an inhibition of neuronal re-uptake of catecholamines (uptake-1), producing an indirect stimulation of cardiac beta 1-receptors. This catecholamine has no effect at alpha 1 and alpha 2-adrenoreceptors, and only very weak and clinically insignificant beta 1-adrenoreceptor agonist activity. Dopexamine hydrochloride improves cardiac performance by a marked vasodilation and a mild inotropic activity. The specific activity at dopaminergic receptors increases cerebral, myocardial, splanchnic and renal blood flows. These haemodynamic effects are associated with an increase in diuresis and natriuresis. These benefits are achieved without side effects such as an increased myocardial oxygen consumption, although induced tachycardia may be responsible for chest pain/anginae pain in patients with ischaemic heart disease. In clinical practice, dopexamine hydrochloride is easy to use; the short plasma half-life (6 minutes in healthy volunteers and 11 minutes in patients with low cardiac output) allows a rapid return to pretreatment status at discontinuation of the infusion. Preliminary studies have shown that dopexamine hydrochloride can produce beneficial effects in patients with acute heart failure or with compromised left ventricular function following cardiac surgery. The drug has also been assessed in patients with septic shock, most often in association with dopamine or norepinephrine. In these patients, dopexamine produces a dose-related increase in cardiac index, stroke volume, heart rate and a decrease in systemic vascular resistance. Its use in this indication must be cautious, particularly in patients with hypotension or decreased venous return. Comparative therapeutic trials are clearly required to establish the efficiency and tolerance of dopexamine hydrochloride in comparison with dopamine and dobutamine, before its place in therapy can fully be defined.
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PMID:[Dopexamine: a new dopaminergic agonist]. 790 85

We studied the acute haemodynamic dose response of nicorandil, a combined nitrate and potassium channel opener, in patients evaluated for chest pain. Single dose oral nicorandil (5, 10, 20, or 30 mg) or placebo was given to 42 right-heart catheterized patients using a randomized block design. Persistent, significant (P < 0.05) haemodynamic changes occurred primarily after 30 mg. Arterial systolic pressure fell significantly after all doses and remained reduced (maximum, 31 mmHg) up to 6 h after 30 mg; heart rate increased significantly up to 1 h. Individual haemodynamic sensitivity varied and three patients (1, 10 mg; 2, 30 mg) developed transient symptomatic hypotension associated with bradycardia. Pulmonary artery systolic pressure (diastolic was unchanged) declined significantly (maximum, 5 mmHg) up to 6 h after 30 mg whereas pulmonary capillary wedge (baseline normal) and mean right atrial pressures decreased transiently. Cardiac index (baseline normal) declined slightly (significantly after 30 mg); however, stroke volume index and stroke work index were significantly and persistently reduced after all doses. Total systemic vascular resistance declined slightly after 30 mg. Individual plasma nicorandil concentrations were variable and systemic bioavailability was reduced compared with values reported in healthy subjects. Nicorandil demonstrated cardiac unloading actions. Variable plasma concentrations, haemodynamic effects, and patient sensitivity warrant low initial doses with individual dose titration, especially if cardiac filling pressures are low.
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PMID:Dose-related haemodynamic effects and pharmacokinetics of oral nicorandil in patients evaluated for chest pain. 807 66

Left ventricular damage by necrosis of myocardial tissue can lead to compromise of left ventricular function, to left ventricular volume increase and ultimately to development of heart failure. This sequence in the pathophysiology has been shown to be blunted by ACE inhibitors. Volume increase, however, can also be helpful in restoring stroke volume and ameliorate elevation of filling pressures. Furthermore, very early institution of ACE inhibition has failed to improve short-term mortality after myocardial infarction in one large trial. The aim of the ECCE trial therefore is, to investigate the early effects of the ACE inhibitor captopril on compromise of exercise capacity, thought to be a first measurable sign of developing heart failure. The ECCE trial is a randomized, seven-center investigation, studying the effects of ACE inhibition on oxygen uptake in a double blind, placebo controlled design in a group of 204 patients. Sample size was calculated on the basis of a pilot trial. The study design and first not unblinded data of 104 patients are presented. The population consists of predominantly male patients with mostly first myocardial infarction. They were admitted to hospital within five hours of onset of chest pain. End-diastolic volumes were normal, but ejection fraction was moderately compromised. ACE inhibition was started after the first day, but within 72 hours of onset of chest pain. After four and after twelve weeks, oxygen uptake was considerably below expected values and one third of the patients had severe compromise of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experiences with ACE inhibitors early after acute myocardial infarction. Rationale and design of the German Multicenter Study on the Effects of Captopril on Cardiopulmonary Exercise parameters post myocardial infarction (ECCE). 812 22

To ascertain whether the outcome of patients with suspected myocardial infarction differs when chest pain is still present at initiation of thrombolytic therapy, participants in the Thrombolysis in Myocardial Infarction Phase II study, all of whom presented within 4 hours of symptoms onset, were retrospectively divided into 2 groups: (1) those with chest pain present at onset of intravenous thrombolysis, n = 3,000; and (2) those who were free of chest pain on beginning intravenous thrombolytic therapy, n = 337. Patients free of chest pain were older (58 vs 57 years, p = 0.01), more often women (23 vs 17%, p = 0.01), had fewer electrocardiographic leads with ST elevation (3.8 vs 4.1, p < 0.001), and the presenting event was confirmed less often as myocardial infarction than as chest pain without infarction (88 vs 96%, p < 0.001). There were no significant differences between the 2 groups for in-hospital death, reinfarction, recurrent ischemic events, stroke, overall hemorrhagic complications, coronary angioplasty or bypass surgery. At 6-weeks follow-up, more pain-free patients had resting ejection fraction > 0.55 (35 vs 31%, p = 0.001) and fewer developed congestive heart failure (12 vs 20%). At 1-year follow-up, fewer pain-free patients developed congestive heart failure (15 vs 21%, p = 0.009), but no differences existed between the 2 groups in frequency of death, reinfarction, coronary angioplasty, bypass surgery or anginal class. Thus, there are several observations in patients who were free of chest pain at onset of lytic therapy. (1) The majority developed enzymatic or electrocardiographic evidence of acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect on outcome of the presence or absence of chest pain at initiation of recombinant tissue plasminogen activator therapy in acute myocardial infarction. The Thrombolysis in Myocardial Infarction Investigators. 816 Jun 7

Long term oral warfarin should be administered to elderly patients with atrial fibrillation who are at high risk for developing thromboembolic stroke and who have no contraindications to anticoagulant therapy. Oral aspirin (acetylsalicylic acid) 325mg daily may be given to elderly patients with chronic atrial fibrillation who have contraindications to anticoagulant therapy or who are not at high risk for developing thromboembolic stroke. Management of atrial fibrillation includes treatment of the underlying disease and precipitating factors. If patients have paroxysmal atrial fibrillation with a very rapid ventricular rate associated with hypotension, severe left ventricular failure or chest pain due to myocardial ischaemia, immediate direct-current cardioversion should be performed. Intravenous verapamil, diltiazem or a beta-blocker should be used for immediate slowing of a very rapid ventricular rate associated with atrial fibrillation. If a rapid ventricular rate associated with atrial fibrillation persists at rest or during exercise despite digoxin, then oral verapamil, diltiazem or a beta-blocker should be added. Low dosages of oral amiodarone (200 to 400 mg/day) may be used in selected patients with symptomatic life-threatening atrial fibrillation refractory to other therapy. No medication which depresses atrioventricular conduction should be given to patients with atrial fibrillation and a slow ventricular rate. Cardioversion should not be performed in asymptomatic elderly patients with chronic atrial fibrillation. This author would use a beta-blocker for control of ventricular arrhythmias and following conversion of atrial fibrillation to sinus rhythm. Should atrial fibrillation recur, beta-blockers have the additional advantage of slowing the ventricular rate.
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PMID:Optimal management of older patients with atrial fibrillation. 819 93

Indicators such as lowering of blood pressure in hypertension, alleviation of chest pain in angina pectoris, improvement in rest or exertional dyspnea from congestive heart failure (CHF) and suppression of ventricular arrhythmia are widely used in the management of cardiovascular diseases. There are often strong associations between the physiological indicators and the long-term clinical outcomes of cardiovascular disease such as stroke, myocardial infarction, sudden death and all-cause mortality. Physicians have assumed reasonably that early improvements in physiological markers will lead invariably to better long-term clinical outcomes. In recent years, a number of large clinical trials have demonstrated that short-term physiological improvements are not necessarily linked to better long-term clinical outcomes, but may be associated with less benefit than expected or even with detrimental outcomes. Management of cardiovascular diseases is complicated by the possibility that beneficial effects of a particular drug may be offset by its negative actions on the cardiovascular system. Effective antihypertensives may depress cardiac contractility; inotropes enhance left ventricular contractility in CHF, but may increase the risk of serious ventricular dysrhythmia; drugs which suppress ventricular arrhythmia may precipitate CHF or even excite pro-arrhythmic effects. Physicians must be conscious of this interplay of potentially beneficial and deleterious effects when cardiovascular drugs are prescribed. It is important in the analysis of large clinical trials of cardiovascular drugs to identify those situations in which the drug exhibits more benefit than harm and to determine, if possible, those aspects of drug action, drug dosage and population characteristics which contribute to the beneficial and detrimental actions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early effects of cardiovascular drugs--do they predict clinical outcomes? 820 69

This study was conducted in 19 hospitals in the metropolitan Seattle area and included 6,270 unselected patients who had acute myocardial infarction (AMI) between January 1988 and April 1991. Hospital mortality was determined and related to patient demographic and clinical characteristics, the use of reperfusion therapies, and to complications after AMI. Thrombolytic therapy or direct coronary angioplasty < 6 hours from symptom onset was used to treat 1,185 (19%) and 524 (9%) patients, respectively. There were 629 (10%) hospital deaths; most occurred during the first 3 days of hospitalization. Factors affecting mortality after admission included: recurrent chest pain, recurrent AMI, development of heart failure, and the occurrence of stroke. After adjustment for age, treatment with thrombolytic therapy or direct angioplasty had no independent effect on reducing the overall mortality rate. Hospital mortality rates for AMI have improved considerably since 1970, although recurrent myocardial ischemic events continue to have an adverse effect on outcome. The current use of reperfusion treatments has had minimal causal impact on overall mortality rates, principally because less than one third of patients, who are relatively "low risk," are eligible and receive these treatments.
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PMID:Hospital mortality in acute myocardial infarction in the era of reperfusion therapy (the Myocardial Infarction Triage and Intervention Project). 821 42

Acute aortic dissection is the most common fatal condition that involves the aorta; nevertheless, despite major advances in noninvasive diagnosis, the correct antemortem diagnosis is made in less than half the cases. To promote continued improvement in the prompt recognition of aortic dissection, we present a review of the Mayo Clinic experience with 235 patients who had 236 substantiated aortic dissections. At the time of initial assessment, 158 patients (67%) had acute and 78 patients (33%) had chronic aortic dissection. Hypertension was the most common predisposing factor (78% of patients overall). The acute onset of severe chest pain was the most common initial complaint (74%), but 33 patients (15%) had painless aortic dissection and abnormal chest roentgenographic findings. Less common manifestations included congestive heart failure, syncope, cerebrovascular accident, shock, paraplegia, and lower extremity ischemia. The initial clinical impression was aortic dissection in 62% of patients overall. In 17 patients (28%), the correct diagnosis was not made before postmortem examination. Although the clinical features of aortic dissection have gained wider appreciation, the diagnosis still remains unsuspected in a substantial number of patients. In a patient who has a catastrophic illness and unexplained symptoms that could be of vascular origin, especially in the presence of chest pain, aortic dissection should always be included in the differential diagnosis.
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PMID:Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990). 1188 38


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