Sex influences the susceptibility to reperfusion-induced sustained ventricular tachycardia and β-adrenergic receptor blockade in conscious rats

2007 ◽  
Vol 293 (5) ◽  
pp. H2799-H2808 ◽  
Author(s):  
Heidi L. Lujan ◽  
Victoria J. Kramer ◽  
Stephen E. DiCarlo
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Adrenergic Receptor ◽  
Left Main Coronary Artery ◽  
Gonadal Hormones ◽  
Receptor Blockade ◽  
Left Main ◽  
Reperfusion Arrhythmias ◽  
Conscious Rats ◽  
Adrenergic Receptor Blockade

Reperfusion after a brief period of cardiac ischemia can lead to potentially lethal arrhythmias. Importantly, there are sex-related differences in cardiac physiology and in the types and severity of cardiac arrhythmias. Therefore, we tested the hypothesis that gonadal hormones influence the susceptibility to reperfusion-induced sustained ventricular tachycardia (VT), as well as the response to β-adrenergic receptor blockade. Male and female intact and gonadectomized rats were instrumented, and arterial pressure, temperature, ECG, and cardiac output were recorded. In addition, a snare was placed around the left main coronary artery. Tension was applied to the snare for determination of susceptibility to sustained VT produced by 3 min of occlusion and reperfusion of the left main coronary artery in conscious rats. Reperfusion culminated in sustained VT in 77% (10 of 13 susceptible) of female rats and 56% (9 of 16 susceptible) of male rats ( P > 0.05, male vs. female). β-Adrenergic receptor blockade prevented sustained VT in females only [1 of 9 susceptible females (11%) vs. 6 of 9 susceptible males (67%), P < 0.05]. Ovariectomy did not significantly reduce the susceptibility to reperfusion arrhythmias [5 of 9 susceptible (56%)]. In sharp contrast, orchidectomy significantly increased the susceptibility to reperfusion arrhythmias [9 of 9 susceptible (100%)]. Finally, β-adrenergic receptor blockade prevented sustained VT in ovariectomized females [0 of 4 susceptible (0%)] and orchidectomized males [0 of 7 susceptible (0%)], but the protective effect of β-blockade was due to a reduction in heart rate in males only. Thus gonadal hormones influence the susceptibility to reperfusion-induced arrhythmias, as well as the effects and mechanisms of β-adrenergic receptor blockade.

Sex differences to myocardial ischemia and β-adrenergic receptor blockade in conscious rats

2008 ◽  
Vol 294 (4) ◽  
pp. H1523-H1529 ◽  
Author(s):  
Heidi L. Lujan ◽  
Stephen E. DiCarlo
Keyword(s):  
Sex Differences ◽  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Arterial Pressure ◽  
Adrenergic Receptor ◽  
Gonadal Hormones ◽  
Sustained Ventricular Tachycardia ◽  
Receptor Blockade ◽  
Conscious Rats ◽  
Adrenergic Receptor Blockade

We recently documented sex differences in the susceptibility to reperfusion-induced sustained ventricular tachycardia and β-adrenergic receptor blockade in conscious rats. However, the effect of sex on ischemia-induced ventricular arrhythmias and β-adrenergic receptor blockade is underinvestigated. Therefore, we tested the hypothesis that gonadal hormones influence the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion as well as the response to β-adrenergic receptor blockade. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Male and female intact and gonadectomized (GnX) rats were instrumented with a radiotelemetry device for recording arterial pressure, temperature, and ECG, as well as a Doppler ultrasonic flow probe to measure cardiac output and a snare around the left main coronary artery. The VAT was determined in conscious rats by pulling on the snare. The VAT was significantly longer in intact females (5.56 ± 0.19) vs. intact males (4.31 ± 0.14 min). This sex difference was abolished by GnX. Specifically, GnX decreased the VAT in females (4.55 ± 0.22) and increased the VAT in males (5.14 ± 0.30 min). Thus male sex hormones increase and female sex hormones decrease the susceptibility to ischemia-induced sustained ventricular tachycardia. β-Adrenergic receptor blockade increased the VAT in intact males and GnX females only. Thus gonadal hormones influence the response to β-adrenergic receptor blockade. Uncovering major differences between males and females in the pathophysiology of the cardiovascular system may result in sex-specific optimization of patient treatments.

T5 spinal cord transection increases susceptibility to reperfusion-induced ventricular tachycardia by enhancing sympathetic activity in conscious rats

2007 ◽  
Vol 293 (6) ◽  
pp. H3333-H3339 ◽  
Author(s):  
Heidi L. Lujan ◽  
Stephen E. DiCarlo
Keyword(s):  
Spinal Cord ◽  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Cause Of Death ◽  
Adrenergic Receptor ◽  
Sympathetic Activity ◽  
Left Main Coronary Artery ◽  
Sustained Ventricular Tachycardia ◽  
Spinal Cord Transection ◽  
Left Main

We recently documented that paraplegia (T5 spinal cord transection) alters cardiac electrophysiology and increases the susceptibility to ventricular tachyarrhythmias induced by programmed electrical stimulation. However, coronary artery occlusion is the leading cause of death in industrially developed countries and will be the major cause of death in the world by the year 2020. The majority of these deaths result from tachyarrhythmias that culminate in ventricular fibrillation. β-Adrenergic receptor antagonists have been shown to reduce the incidence of sudden cardiac death. Therefore, we tested the hypothesis that chronic T5 spinal cord transection increases the susceptibility to clinically relevant ischemia-reperfusion-induced sustained ventricular tachycardia due to enhanced sympathetic activity. Intact and chronic (4 wk after transection) T5 spinal cord-transected (T5X) male rats were instrumented to record arterial pressure, body temperature, and ECG. In addition, a snare was placed around the left main coronary artery. The susceptibility to sustained ventricular tachycardia produced by 2.5 min of occlusion and reperfusion of the left main coronary artery was determined in conscious rats by pulling on the snare. Reperfusion culminated in sustained ventricular tachycardia in 100% of T5X rats (susceptible T5X, 10 of 10) and 0% of intact rats [susceptible intact, 0 of 10 ( P < 0.05, T5X vs. intact)]. β-Adrenergic receptor blockade prevented reperfusion-induced sustained ventricular tachycardia in T5X rats [susceptible T5X 0 of 8, 0% ( P < 0.05)]. Thus paraplegia increases the susceptibility to reperfusion-induced sustained ventricular tachycardia due to enhanced sympathetic activity.

scholarly journals Left anterior descending coronary artery dissection during ventricular tachycardia ablation – case report

2018 ◽  
Vol 56 (1) ◽  
pp. 63-66
Author(s):  
Kresimir Kordic ◽  
Sime Manola ◽  
Ivan Zeljkovic ◽  
Ivica Benko ◽  
Nikola Pavlovic
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Left Main Coronary Artery ◽  
Left Ventricular ◽  
Artery Dissection ◽  
Complication Rates ◽  
Left Main ◽  
Coronary Artery Dissection ◽  
Ventricular Tachycardia Ablation ◽  
First Case

Abstract Fascicular left ventricular tachycardia (VT) is the second most frequent idiopathic left VT in the setting of a structurally normal heart. Catheter ablation is curative in most patients with low complication rates. We report a case of ostial left anterior descending coronary artery (LAD) occlusion during fascicular ventricular tachycardia ablation. Dissection was the most likely cause of LAD obstruction. To the authors’ best knowledge, this is the first case reporting selective LAD dissection during electrophysiology study with no left main coronary artery (LMCA) affection.

scholarly journals Influence of myocardial oxygen demand on the coronary vascular response to arterial blood gas changes in humans

2018 ◽  
Vol 315 (1) ◽  
pp. H132-H140 ◽  
Author(s):  
Tyler D. Vermeulen ◽  
Lindsey M. Boulet ◽  
Mike Stembridge ◽  
Alexandra M. Williams ◽  
James D. Anholm ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Adrenergic Receptor ◽  
Blood Velocity ◽  
Rate Pressure Product ◽  
Receptor Blockade ◽  
Vascular Response ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
The Mean ◽  
Adrenergic Receptor Blockade

It remains unclear if the human coronary vasculature is inherently sensitive to changes in arterial Po2 and Pco2 or if coronary vascular responses are the result of concomitant increases in myocardial O2 consumption/demand ([Formula: see text]). We hypothesized that the coronary vascular response to Po2 and Pco2 would be attenuated in healthy men when [Formula: see text] was attenuated with β1-adrenergic receptor blockade. Healthy men (age: 25 ± 1 yr, n = 11) received intravenous esmolol (β1-adrenergic receptor antagonist) or volume-matched saline in a double-blind, randomized crossover study and were exposed to poikilocapnic hypoxia, isocapnic hypoxia, and hypercapnic hypoxia. Measurements made at baseline and after 5 min of steady state at each gas manipulation included left anterior descending coronary blood velocity (LADV; Doppler echocardiography), heart rate, and arterial blood pressure. LADV values at the end of each hypoxic condition were compared between esmolol and placebo. The rate-pressure product (RPP) and left ventricular mechanical energy (MELV) were calculated as indexes of [Formula: see text]. All gas manipulations augmented RPP, MELV, and LADV, but only RPP and MELV were attenuated (4–18%) after β1-adrenergic receptor blockade ( P < 0.05). Despite attenuated RPP and MELV responses, β1-adrenergic receptor blockade did not attenuate the mean LADV vasodilatory response compared with placebo during poikilocapnic hypoxia (29.4 ± 2.2 vs. 27.3 ± 1.6 cm/s) and isocapnic hypoxia (29.5 ± 1.5 vs. 30.3 ± 2.2 cm/s). Hypercapnic hypoxia elicited a feedforward coronary dilation that was blocked by β1-adrenergic receptor blockade. These results indicate a direct influence of arterial Po2 on coronary vascular regulation that is independent of [Formula: see text]. NEW & NOTEWORTHY In humans, arterial hypoxemia led to an increase in epicardial coronary artery blood velocity. β1-Adrenergic receptor blockade did not diminish the hypoxemic coronary response despite reduced myocardial O2 demand. These data indicate hypoxemia can regulate coronary blood flow independent of myocardial O2 consumption. A plateau in the mean left anterior descending coronary artery blood velocity-rate-pressure product relationship suggested β1-adrenergic receptor-mediated, feedforward epicardial coronary artery dilation. In addition, we observed a synergistic effect of Po2 and Pco2 during hypercapnic hypoxia.

scholarly journals Recurrent Syncope Attributed to Left Main Coronary Artery Severe Stenosis

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Min Li ◽  
Xinyi Zheng ◽  
Hua Liu ◽  
Yujie Liu
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Ventricular Arrhythmia ◽  
Left Main Coronary Artery ◽  
Heart Rhythm ◽  
Coronary Intervention ◽  
Left Main ◽  
Coronary Syndrome ◽  
Coronary Angiograph

Patients with acute coronary syndrome (ACS) rarely manifest as recurrent syncope due to malignant ventricular arrhythmia. We report a case of a 56-year-old Chinese male with complaints of paroxysmal chest burning sensation and distress for 2 weeks as well as loss of consciousness for 3 days. The electrocardiogram (ECG) revealed paroxysmal multimorphologic ventricular tachycardia during attack and normal heart rhythm during intervals. Coronary angiograph showed 90% stenosis in left main coronary artery and 80% stenosis in anterior descending artery. Two stents sized4.0*18 mm and2.75*18 mm were placed at left main coronary artery and anterior descending artery, respectively, during percutaneous coronary intervention (PCI). The patient was discharged and never had ventricular arrhythmia again during a 3-month follow-up since the PCI. This indicated that ventricular tachycardia was correlated with persistent severe myocardial ischemia. Coronary vasospasm was highly suspected to be the reason of the sudden attack and acute exacerbation. PCI is recommended in patients with both severe coronary artery stenosis and ventricular arrhythmia. Removing myocardial ischemia may stop or relieve ventricular arrhythmia and prevent cardiac arrest.

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