Exercise-induced left bundle branch block and propafenone administration.
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Biomedical subjects
Publications and source records attributed to Andreas Michaelides.
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OBJECTIVES: Erectile dysfunction (ED) shares common risk factors with coronary artery disease (CAD). It has been suggested that ED may be considered a clinical manifestation of a generalized vascular disease affecting also the penile arteries. The aim of this prospective study was to evaluate angiographically the incidence of asymptomatic CAD in men with ED of vascular origin. METHODS: Fifty consecutive asymptomatic men, aged 41-74 years, with non-psychogenic and non-hormonal ED were comprehensively evaluated using medical history and examination, exercise treadmill test and stress echocardiography. Patients who had positive one or both of the two non-invasive procedures were referred for coronary arteriography in order to document CAD and evaluate the severity of the disease. RESULTS: The mean time interval between the onset of ED and cardiological assessment was 25 months (range 1-66). Smoking (32 patients/64%), hypertension (31 patients/62%) and hyperlipidemia (26 patients/52%) were the most common risk factors. Moreover, 35 men (70%) had two or more risk factors. Twelve patients (24%) with ED had positive one or both of the two non-invasive procedures and one patient presented with acute myocardial infarction before he completed the non-invasive investigation. Coronary arteriography performed in ten patients (in nine with positive one or both of the two non-invasive procedures [while the other three refused], and in the patient with acute myocardial infarction) demonstrated that one patient had three-vessel disease, two patients had two-vessel disease and six patients had single-vessel disease. CONCLUSIONS: A considerable proportion (9/47 or 19%) of patients with ED of vascular origin has angiographically documented silent CAD. These findings support the strategy that patients with ED should undergo further cardiovascular evaluation.
OBJECTIVE: It is known that exercise-induced ischemia in patients with coronary artery disease (CAD) may produce QRS prolongation in the surface electrocardiogram (ECG). To investigate the presence of exercise-induced Q-wave prolongation in patients with single-vessel CAD and Q-wave myocardial infarction (MI), in association with the presence of reversible perfusion defects during thallium scintigraphy in the infarcted area. METHODS: 107 consecutive patients (89 males, mean age 56+/-8 years) were evaluated. All patients underwent coronary arteriography, maximal treadmill exercise testing and thallium-201 scintigraphy. Q-wave duration was measured both before exercise testing and during maximal heart rate from 12-lead ECGs recorded with a paper speed of 50 mm/s. RESULTS: Only 57 out of the 107 studied patients showed reversible perfusion defects in the infarcted area during thallium scintigraphy. Q-wave duration was significantly increased from the resting to the stress ECG (DeltaQ-wave duration) in patients with reversible perfusion defects in the infarcted areas (10+/-13 ms), but not in patients with fixed defects in the infarcted zone (-2.0+/-5 ms, p<0.01). The sensitivities and the specificities of Q-wave prolongation, ST segment elevation, and the combination of ST segment elevation with ST segment depression in the reciprocal leads for the detection of myocardial viability in the infarcted area were 82%, 48%, 29% and 88%, 50%, and 90%, respectively. CONCLUSIONS: Exercise-induced Q-wave prolongation is demonstrated in those patients with single-vessel CAD and a recent MI who show reversible perfusion defects in thallium scintigraphy. Exercise-induced Q-wave prolongation was found to be a sensitive and specific ECG marker for the detection of myocardial viability in the infarcted area.
Recently a growing amount of interest has been focused on new risk factors for cardiovascular disease, such as insulin, leptin, homocysteine, and urinary albumin excretion (UAE). Furthermore, the absence of a nocturnal blood pressure (BP) decrease is emerging as an index for future target organ damage. In the present study we aimed to determine the relationship between these risk factors and circadian BP variations in essential hypertensive subjects. One hundred six patients, aged 54+/-7 years, with stage I-II untreated hypertension were classified as dippers and nondippers according to the diurnal variation of >10% between mean daytime and nighttime systolic BP (SBP) and diastolic BP (DBP) in 24-h noninvasive ambulatory BP monitoring. Venous blood samples were drawn for determination of insulin, leptin, and homocysteine plasma levels, whereas UAE was evaluated in three consecutive 24-h urine samples. Nondippers compared to dippers had significantly greater hemodynamic load and higher UAE (by 17 mg/24 h, P < .05). The two groups did not differ regarding serum insulin, plasma leptin, and homocysteine levels. In the entire population, leptin was positively correlated with age, body mass index, 24-h DBP, fasting serum insulin, and plasma homocysteine levels, whereas homocysteine levels were significantly related to 24-h SBP and DBP values. Multiple linear regression analyses revealed that only UAE was significantly related with nocturnal SBP and DBP decrease (P < .05 for both). These findings suggest that the increased UAE observed in nondipper hypertensive subjects possibly represents a useful indicator-for future target organ damage.