The relation between endothelial dependent flow mediated dilation of the brachial artery and coronary collateral development – a cross sectional study

<p>Abstract</p> <p>Background</p> <p>Endothelial dysfunction is thought to be a potential mechanism for the decreased presence of coronary collaterals. The aim of the study was to investigate the association between systemic endothelial function and the extent of coronary collaterals.</p> <p>Methods</p> <p>We investigated the association between endothelial function assessed via flow mediated dilation (FMD) of the brachial artery following reactive hyperemia and the extent of coronary collaterals graded from 0 to 3 according to Rentrop classification in a cohort of 171 consecutive patients who had high grade coronary stenosis or occlusion on their angiograms.</p> <p>Results</p> <p>Mean age was 61 years and 75% were males. Of the 171 patients 88 (51%) had well developed collaterals (grades of 2 or 3) whereas 83 (49%) had impaired collateral development (grades of 0 or 1). Patients with poor collaterals were significantly more likely to have diabetes (<it>p </it>= 0.001), but less likely to have used statins (<it>p </it>= 0.083). FMD measurements were not significantly different among good and poor collateral groups (11.5 ± 5.6 vs. 10.4 ± 6.2% respectively, <it>p </it>= 0.214). Nitroglycerin mediated dilation was also similar (13.4 ± 5.9 vs. 12.8 ± 6.5%, <it>p </it>= 0.521).</p> <p>Conclusion</p> <p>No significant association was found between the extent of angiographically visible coronary collaterals and systemic endothelial function assessed by FMD of the brachial artery.</p

Acute alcohol intake and QT dispersion in healthy subjects.

Objective: QT dispersion (QTd) is the maximal interlead difference in the QT interval on the surface 12-lead electrocardiogram (ECG). An increase in QTd is found in patients with various cardiac diseases and reflects cardiac autonomic imbalance. Variability of QT duration among the 12 surface ECG leads expresses electrical instability and greater susceptibility to malignant ventricular arrhythmias. Electrophysiological studies have shown that heavy episodic drinking facilitates the induction of ventricular tachyarrhythmias in some heavy drinkers. However, the association between QTd and acute alcohol intake has not been studied previously in healthy subjects. Method: In a randomized crossover study, 10 healthy male volunteers (average [SD] age 30 [2.1] years, range: 25-33) received either alcohol (six 12-oz cans of beer) or placebo (juice). The alcohol group consumed 0.97 [0.12] g/kg body weight ethanol, and the placebo group consumed the same amount of juice in a 1-hour period. After a 48-hour washout period, the alcohol group drank juice, and the juice group drank alcohol. QTd and corrected QTd (cQTd) were measured in a baseline ECG after the alcohol period (AP) and after the juice period (JP). Results: In comparison with baseline ECG (31.7 [9.4] ms), QTd values after AP (42.1 [10.8] ms) were significantly prolonged (p = .027), but this was not so after JP (33.8 [7.1] ms; p = NS). Also in comparison with baseline ECG (35.7 [11.1] ms), cQTd values after the AP (49.8 [12.7] ms) were significantly prolonged (p = .005), but again, this was not so after the JP (36.8 [7.3] ms; p = NS). Conclusions: Heavy episodic drinking is associated with an increase in QTd and cQTd

Acute alcohol intake and QT dispersion in healthy subjects

Objective: QT dispersion (QTd) is the maximal interlead difference in the QT interval on the surface 12-lead electrocardiogram (ECG). An increase in QTd is found in patients with various cardiac diseases and reflects cardiac autonomic imbalance. Variability of QT duration among the 12 surface ECG leads expresses electrical instability and greater susceptibility to malignant ventricular arrhythmias. Electrophysiological studies have shown that heavy episodic drinking facilitates the induction of ventricular tachyarrhythmias in some heavy drinkers. However, the association between QTd and acute alcohol intake has not been studied previously in healthy subjects. Method: In a randomized crossover study, 10 healthy male volunteers (average [SD] age 30 [2.1] years, range: 25-33) received either alcohol (six 12-oz cans of beer) or placebo (juice). The alcohol group consumed 0.97 [0.12] g/kg body weight ethanol, and the placebo group consumed the same amount of juice in a 1-hour period. After a 48-hour washout period, the alcohol group drank juice, and the juice group drank alcohol. QTd and corrected QTd (cQTd) were measured in a baseline ECG after the alcohol period (AP) and after the juice period (JP). Results: In comparison with baseline ECG (31.7 [9.4] ms), QTd values after AP (42.1 [10.8] ms) were significantly prolonged (p = .027), but this was not so after JP (33.8 [7.1] ms; p = NS). Also in comparison with baseline ECG (35.7 [11.1] ms), cQTd values after the AP (49.8 [12.7] ms) were significantly prolonged (p = .005), but again, this was not so after the JP (36.8 [7.3] ms; p = NS). Conclusions: Heavy episodic drinking is associated with an increase in QTd and cQTd

The relationship between coronary collateral artery development and inflammatory markers

Objective: This study aims to show the effect of myeloperoxidase (MPO), hsCRP, TNF-alpha values and leukocyte count on the development of coronary collateral arteries in patients with severely diseased coronary arteries. Methods: Current study is an observational cross-sectional study. In the study, 295 patients who had functional obstruction or total coronary occlusion at least 1 month on their angiograms were included. We divided the study population into two groups according to their collateral grade as good collateral (Group 1) (169 patients) and poor collateral (Group 2) (126 patients). Multiple logistic regression analysis was used for independent variables associated with the coronary collateral grade. Results: History of stable angina pectoris was statistically more prevalent in good collateral group (61.5% and 48.4%, p=0.025). Furthermore, MPO activation was higher in good collateral group and the difference was statistically significant (3.7 U/mL and 3.0 U/mL p=0.001). In multiple logistic regression analysis, stable angina pectoris [OR 1.7, 95% CI (1.05-2.8), p=0.03] and high MPO levels [OR 2.7, 95% CI (1.7-4.3), p<0.001] were found to be independent predictors of good collateral development. Conclusion: We think that proinflammatory enzymes and cytokines released from these cells rather than inflammatory cells themselves may play an important role on the collateral development