Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage.

Object: Subarachnoid hemorrhage (SAH) has been associated with cardiac injury and left ventricular (LV) dysfunction. The incidence and natural history of neurocardiogenic injury after SAH remains poorly understood. The objective of this study was to describe the incidence, time course, recovery rate, and segmental patterns of LV dysfunction after SAH.

Acute neurocardiogenic injury after subarachnoid hemorrhage.

Background: Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals.

Methods And Results: For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[(123)I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively.

Treating heart failure with enhanced external counterpulsation (EECP): design of the Prospective Evaluation of EECP in Heart Failure (PEECH) trial.

Background: Enhanced external counterpulsation (EECP) treatment can improve exercise tolerance in patients with ischemic heart disease; however, the possible benefits of EECP in patients with stable heart failure (HF) and left ventricular dysfunction (LVD) are unclear. An open pilot study showed significant increases in exercise tolerance in HF patients undergoing EECP. Thus a larger, controlled study of EECP in patients with stable HF (New York Heart Association [NYHA] classes II and III) and LVD was undertaken.

Predictors of neurocardiogenic injury after subarachnoid hemorrhage.

Background And Purpose: Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause.

A calcium antagonist vs a non-calcium antagonist hypertension treatment strategy for patients with coronary artery disease. The International Verapamil-Trandolapril Study (INVEST): a randomized controlled trial.

Context: Despite evidence of efficacy of antihypertensive agents in treating hypertensive patients, safety and efficacy of antihypertensive agents for coronary artery disease (CAD) have been discerned only from subgroup analyses in large trials.

Objective: To compare mortality and morbidity outcomes in patients with hypertension and CAD treated with a calcium antagonist strategy (CAS) or a non-calcium antagonist strategy (NCAS).

Design, Setting, And Participants: Randomized, open label, blinded end point study of 22 576 hypertensive CAD patients aged 50 years or older, which was conducted September 1997 to February 2003 at 862 sites in 14 countries.

Second hand smoke stimulates tumor angiogenesis and growth.

Exposure to second hand smoke (SHS) is believed to cause lung cancer. Pathological angiogenesis is a requisite for tumor growth. Lewis lung cancer cells were injected subcutaneously into mice, which were then exposed to sidestream smoke (SHS) or clean room air and administered vehicle, cerivastatin, or mecamylamine.

Comparative effects of aspirin with ACE inhibitor or angiotensin receptor blocker on myocardial infarction and vascular function.

Objectives: We previously showed that an angiotensin-converting enzyme inhibitor (captopril) or an angiotensin receptor blocker (losartan) reduced infarct size and improved endothelial function in a rat model of ischaemia-reperfusion. The present study was undertaken to see if aspirin (ASA) antagonised the beneficial effects of captopril or losartan.

Methods: One hundred and fourteen Sprague-Dawley rats were randomised into six groups; Control, ASA, captopril, losartan, ASA+captopril, and ASA+losartan.

The renin-angiotensin system does not contribute to the endothelial dysfunction and increased infarct size in rats exposed to second hand smoke.

Introduction: Both second hand smoke (SHS) and the renin-angiotensin system (RAS) contribute to endothelial dysfunction and increased infarct size in a rat ischaemia-reperfusion model. However, the potential interaction between SHS and the RAS is unknown.

Methods: Eighty-four rats were randomised into four groups: group C was a normal control; L was given 40 mg/kg/day of losartan in drinking water; SC and SL were exposed to SHS (smoking chamber) and given regular water or 40 mg/kg/day of losartan in drinking water, respectively.

Effects of different durations of pretreatment with losartan on myocardial infarct size, endothelial function, and vascular endothelial growth factor.

A previous study by our group showed that 10 weeks of pretreatment with losartan reduced myocardial infarct size and arrhythmias in a rat model of ischaemia-reperfusion. However, the effect of a differing time course of pretreatment has not been investigated. 104 Sprague-Dawley rats were randomised to four groups: a control, and three treatment groups in which losartan (40 mg/kg/day) was administered in drinking water for one day, one week, and four weeks respectively.

Secondhand tobacco smoke impairs rabbit pulmonary artery endothelium-dependent relaxation.

Objectives: To determine whether secondhand smoke (SHS) induces pulmonary artery endothelial dysfunction, and whether dietary L-arginine supplementation is preventive.

Background: SHS causes coronary and peripheral arterial endothelial dysfunction.

Methods: The effects of L-arginine supplementation (2.

Comparative effects of ACE inhibitors and an angiotensin receptor blocker on atherosclerosis and vascular function.

Background: Both angiotensin-converting enzyme inhibitors (ACE-I(s)) and angiotensin receptor blockers (ARB(s)) provide vascular protection. This study was designed to compare ACE-I(s) with widely differing tissue affinity (captopril and quinapril) and an ARB (losartan) on vascular protection against the adverse effects of high cholesterol.

Methods And Results: Forty-two New Zealand rabbits on a 0.