Search

Objectives. Our aim was to test the hypothesis that increased beat to beat morphologic variations in the body surface electrocardiogram (ECG) are associated with fragmented diastolic electrical activity that appears after coronary artery ligation and to correlate the appearance of spontaneous ventricular fibrillation after coronary ligation with the magnitude of the ECG beat to beat variability. Background. Unstable and variably delayed electrical activation precedes the development of ventricular fibrillation in dogs with acute ischemia. Detection of these highly variable low amplitude signals from the body surface is currently impossible. We have developed a system designed to measure the degree of beat to beat variability of the ECG. Methods. With high fidelity electrocardiography, subtle beat to beat ECG morphologic variations were detected in epicardial and body surface electrograms and quantified as the variance of the ECG voltage at specific points of the cardiac cycle. The ratio of the variance at the QRS offset to that of the QRS onset (beat to beat variability index) was then calculated. Results. Ventricular fibrillation developed in 12 of 27 dogs after left anterior descending coronary artery ligation. In 7 of the 12 dogs it occurred immediately (

To the Editor: Chronic hypertension is associated with arterial endothelial dysfunction, the precursor to atherosclerosis ([1][1]); however, less is known about the effects of brief episodes of hypertension on endothelial function. Lamping and Dole ([2][2]) demonstrated that

Our laboratory has previously demonstrated that nitric oxide (NO) mediates coronary arteriolar dilation to increased myocardial oxygen consumption (MVO 2 ). NO mediated dilation has been shown to be attenuated in diabetes (DM), and endoperoxide antagonists restore this dilation to normal. We, therefore, studied the effect of DM on metabolically mediated dilation of coronary arterioles. We further tested the effect of S029548 (SQ; thromboxane A2 and prostaglandin H2 receptor antagonist) on coronary arteriolar dilatory responses to increased MVO 2 in DM. We measured changes in epicardial arteriolar diameters in 5 DM (1 week alloxan, 60 mg/kg, iv), 4 DM after administration of SQ (2 mg/kg. iv), and 6 normal dogs during increased MVO 2 , using dobutamine (DOB; 10 μ g/kg/min, iv) with rapid atrial pacing (RAP; 288 ± 4 bpm). Diameters were measured using intravital microscopy in anesthetized dogs with stroboscopic epi-illumination coupled to the cardiac cycle. Mean aortic pressure and blood gases were monitored and kept constant throughout the protocol. Results Control DOB DOB + RAP MVO 2 diameter ( μ m) MVO 2 %Δin diameter MVO 2 %Δin diameter Normal 11 ± 1 60 ± 5 23 ± 2 24 ± 4 39 ± 7 43 ± 6 OM 21 ± 7 78 ± 6 36 ± 13 17 ± 5 40 ± 13 14 ± 3 * OM + SQ 16 ± 3 82 ± 9 22 ± 1 20 ± 3 41 ± 5 37 ± 7 mean ± SEM, * P l 0.05 vs. Normal. MVO 2 is ml/min/100 g In DM animals, during DOB + RAP, arterial-venous oxygen difference increased as flow decreased, thus keeping MVO 2 similar. Thus, coronary arterioles in diabetes demonstrate attenuated microvascular dilation to increased myocardial oxygen consumption, and vasoconstrictor endoperoxides playa key role in this impaired response.