Chronic hypertension and left ventricular hypertrophy facilitate induction of sustained ventricular tachycardia in dogs 3 hours after left circumflex coronary artery occlusion

The purpose of this study was to investigate the electrophysiology of acute ischemia in hypertrophic as compared with nonhypertrophic myocardium. Left circumflex coronary artery occlusion was produced in anesthetized open chest dogs. Of 40 dogs studied, 22 were normotensive and 18 had chronic hypertension produced by a single kidney renal clamp procedure. Recordings of electrograms and extrastimulus testing were performed in endocardial and epicardial sites in both normal and ischemically damaged zones documented by triphenyltetrazolium chloride. In the hypertrophy group, there was greater endocardial to epicardial conduction delay in ischemic zones, mean +/- SEM 57 +/- 4 ms versus 31 +/- 2 ms in the normotensive group (p less than 0.05). Also, sustained monomorphic ventricular tachycardia was inducible in seven of eight dogs with hypertrophy and in none of eight normotensive dogs surviving to 3 h. Entrainment and several observations during induction were consistent with reentrant ventricular tachycardia. To exclude hypertension alone as an etiology of tachycardia, five normotensive dogs without inducible monomorphic tachycardia remained unchanged during hypertension produced with low doses of phenylephrine or descending aortic occlusion. Thus, the electrophysiologic response to ischemia is altered in hypertrophied myocardium, which predisposes to rapid sustained monomorphic ventricular tachycardia.     

Autonomic nervous system activity and the spontaneous initiation of ventricular tachycardia

Objectives. We hypothesized that neurohormonal activity contributes to the initiation of sustained ventricular tachycardia (VT) as reflected in indices of heart rate variability (HRV).

Background. Autonomic nervous system activity participates in experimental arrhythmias but clinical studies have been inconsistent.

Methods. Holter electrocardiograms from 53 patients with VT were analyzed. Heart rate variability indices were determined over 5 and 15 min and 24 h and examined for changes before the onset of VT. Heart rate variability indices in the frequency domain included ultra low frequency power (FP) (ULFP): 0–0.0033 Hz; very low FP (VLFP): 0.0033–0.04 Hz; low FP (LFP): 0.04–0.15 Hz; high FP (HFP): 0.15–0.4 Hz; total power (TP); normalized LFP (LFP_n); normalized HFP (HFP_n), and the ratio: LFP/HFP.

Results. Heart rate variability indices were severely diminished: TP: 12,009 ± 11,076 ms²; ULFP: 10,087 ± 9,565 ms²; VLFP: 1,416 ± 1,571 ms²; LFP: 544 ± 620 ms²; HFP: 161 ± 176 ms², and LFP/HFP: 3.68 ± 2.83. Heart rate increased before VT (80.4 ± 17.3 to 85.3 ± 17.4 bpm, p < 0.001). Several HRV variables declined 30 min before VT compared to 24-h values (VLFP: −5.89 ± 17.81%, p = 0.031; LFP: −5.23 ± 14.3%, p = 0.003; HFP: −4.35 ± 13.7%, p = 0.04). LFP_n and the LFP/HFP ratio decreased significantly before the onset of VT (−17.7 ± 46.9%, p = 0.035 and −8.24 ± 38.8%, p = 0.037, respectively), whereas HFP_n increased slightly (4.29 ± 29.9%, p = 0.097).

Conclusions. Heart rate rose, whereas LFP, LFP_n and LFP/HFP fell before the onset of VT. This pattern of changes could be explained by a rise in sympathetic activity and saturation of the HRV signal resulting in dissociation of the average and rhythmical effects of sympathetic activity. These findings suggest that alterations in autonomic activity contributed to arrhythmogenesis in this group of patients.     

Autonomic control of ventricular tachycardia: direct effects of beta-adrenergic blockade in 24 hour old canine myocardial infarction

The purpose of this study was to determine whether alpha- or beta-adrenergic influences directly modulate the rate of spontaneous ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Chloralose-anesthetized, open chest dogs (n = 41) with ventricular tachycardia were studied. The left anterior descending artery was cannulated distally. Neither intracoronary saline solution nor phenylephrine (0.3 to 12 micrograms) changed the rate of ventricular tachycardia; however, isoproterenol (0.01 to 10 micrograms) produced dose-dependent increases in the rate. In six dogs, metoprolol, 5 mg given intravenously, slowed ventricular tachycardia from 174 +/- 10 (mean +/- SE) to 140 +/- 17 beats/min (p less than 0.05). This was accompanied by decreases in mean arterial pressure from 106 +/- 7 to 95 +/- 8 mm Hg, cardiac output from 2.6 +/- 0.3 to 1.6 +/- 0.3 liters/min and prolongation of atrioventricular conduction from 134 +/- 10 to 189 +/- 29 ms (all p less than 0.05) during atrial pacing at a cycle length of 300 ms. In 10 dogs, metoprolol (0.5 mg) given intracoronary, a dose that shifted the isoproterenol dose-response curve to the right, slowed ventricular tachycardia from 174 +/- 7.2 to 140 +/- 9.7 beats/min (p less than 0.05) without hemodynamic changes. Additional metoprolol (4.5 mg) given intravenously produced hemodynamic alterations, but ventricular tachycardia did not slow further. Therefore, beta- but not alpha-adrenergic influences control the rate of ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Furthermore, beta-adrenergic blockade slows ventricular tachycardia solely by a direct electrophysiologic effect on the tachycardia foci and not indirectly as a result of hemodynamic effects.     

Long term spontaneous evolution of left ventricular function after experimental acute coronary occlusion

In a canine model of acute occlusion of the left anterior descending artery (LAD), left ventriculography was performed before and immediately after occlusion and also one and three weeks later. Regional left ventricular function was evaluated by the centreline method. Global and regional left ventricular function were significantly depressed immediately after occlusion and showed no significant recovery after one and three weeks, except for a decrease in the paradoxical motion of the LAD territory, which was probably due to stiffening of the infarct area.     

Influence of sympathetic tone on ventricular fibrillation threshold during experimental coronary occlusion.

The effects of increased and decreased cardiac sympathetic tone and coronary occlusion on ventricular fibrillation were determined in 14 open chest dogs anesthetized with sodium pentobarbital. Heart rate was kept constant by pacing the right atrium at cycle lengths of 500 msec. Ventricular fibrillation threshold was measured by delivering 350 msec trains of constant current stimuli with a frequency of 100 hertz and 2 msec duration. The minimal current of the train that induced fibrillation was taken as the ventricular fibrillation threshold. In seven animals, the effects of stellate stimulation were studied. Ventricular fibrillation threshold was measured during control periods, after 2 minutes of cornoary occlusion, after 2 minutes of stellate stimulation and after 2 minutes of stellate stimulation and coronary occlusion. Coronary occlusion alone decreased ventricular fibrillation threshold an average of 35 percent of control valvues and stellate stimulation alone decreased the threshold an average of 42 percent of control values. The combination of both these interventions decreased ventricular fibrillation threshold an average of 63 percent of control values. The effects of stellate ablation were studied in seven animals. Ventricular fibrillation threshold was measured during control periods, and during coronary occlusion before and after stellate ganglionectomy. Stellectomy increased the threshold an average of 31 percent above control values. After stellectomy, coronary occlusion decreased ventricular fibrillation threshold by only 11 percent of control values, a value 26 percent higher than the threshold during coronary occlusion before stellectomy. These findings may have therapeutic implications for the management of arrhythmias in patients with acute myocardial infarction or some forms of central nervous system disease.     

Sustained limitation of myocardial necrosis 24 hours after coronary artery occlusion: Verapamil infusion in dogs with small myocardial infarcts

Studies were undertaken to ascertain whether verapamil infusion affords a sustained limitation of myocardial injury in the dog after a 24-hour period of coronary artery occlusion. Regional myocardial ischemia was induced by an embolization procedure which did not involve thoracotomy. Immediately after embolization radioactive microspheres were administered intraventricularly to define any area of myocardial underperfusion (zone at risk of infarction). Verapamil (0.005 mg/kg/min) was then administered and maintained for 24 hours during which time the dogs were allowed to recover from anesthesia. The control group received a corresponding infusion of saline solution. After 24 hours the dogs were killed and transverse myocardial sections (3 mm) were prepared. The resulting area of necrosis was visualized by tetrazolium staining, and risk zones were visualized by autoradiography. In the control heart, 62 ± 7% of the zone at risk deteriorated to necrotic tissue, whereas in the verapamil-treated group only 18 ± 4% of the tissue in the zone at risk became necrotic. Verapamil appeared to exert a significant (p < 0.001) tissue-sparing effect that was sustained for at least 24 hours after the onset of ischemia.     

The initiation of ventricular tachycardia and fibrillation in experimental coronary artery occlusion

Ninety-four dogs were studied electrocardiographically following acute occlusion of the circumflex branch of the left coronary artery in an attempt to elucidate the electrogenesis of ventricular arrhythmias.

In terminal ventricular fibrillation, T wave interruption was invariably present, occurring at the peak or on the downslope of the T wave, and was progressively greater in two thirds of the recorded episodes. In nonterminal ventricular tachycardia, T wave cutoff (present in only one fourth of the episodes) was found near the end of the T wave and was progressively less in successive cardiac cycles.

The commonest type of T wave interruption associated with ventricular arrhythmias occurred when an extrasystolic T wave was interrupted by the QRS of the succeeding ventricular extrasystole (V by V type). This was not seen in isolated ventricular premature beats.

The drop in arterial pressure was quantitatively related to the degree of T wave interruption.     

Pacing termination of spontaneous ventricular tachycardia in the coronary care unit.

We reviewed our experience with the use of pacing techniques in the acute treatment of spontaneous ventricular tachycardia occurring outside the context of acute myocardial ischaemia. Over a consecutive 18 month period 23 patients (20 male, aged 38-76 yr) admitted to our coronary care unit experienced a total of 75 episodes of haemodynamically tolerated sustained ventricular tachycardia. Pace termination was attempted in 18 patients in a total of 58 episodes of ventricular tachycardia using a standard temporary external pacemaker. Pacing was successful in 32/58 (55%) attempts vs 13/49 (27%) with intravenous antiarrhythmic drug therapy p = 0.003. The superior success rate of pacing was apparent whether or not patients were receiving chronic antiarrhythmic drug therapy. Pace termination should be considered in the treatment of haemodynamically tolerated spontaneous ventricular tachycardias.     

Severe infundibular pulmonary stenosis and coronary artery stenosis with ventricular tachycardia 24 years after mediastinal irradiation

A 28-year-old man developed severe infundibular pulmonary stenosis (PS), coronary artery stenosis with sustained ventricular tachycardia (VT) 24 years after mediastinal irradiation (total amount of 40 Gray) for non-Hodgkin's lymphoma. Repair of right ventricular outflow tract and coronary artery bypass graft procedure were performed. Infundibular PS was successfully relieved after operation and VT was also controlled by medication. Mediastinal irradiation often causes various cardiac complications after a latent period. Therefore, continuous careful observation is mandatory in patients with the history of mediastinal irradiation.     

Sustained beneficial effects of gallopamil (D600) on size of myocardial infarction 24 hours after coronary artery occlusion in dogs

To examine whether gallopamil (D600), a methoxy derivative of verapamil, has sustained beneficial effects on the ischemic myocardium, its effects on the size of myocardial infarction determined 6 hours (protocol 1) and 24 hours (protocol 2) after left anterior descending coronary artery occlusion were compared in anesthetized, open-chest dogs. To quantify the extent of the hypoperfused zone, Tc-99m- or In-111-albumin microspheres were injected into the left atrium 1 minute after occlusion. Fifteen minutes after occlusion, dogs were randomly assigned to a control group or a gallopamil-treated group that received immediately after assignment 0.08 mg/kg of gallopamil followed by a continuous infusion of 0.2 mg/kg/hr for 6 hours. Six or 24 hours after occlusion, the left ventricle was cut into 3 mm thick slices for triphenyltetrazolium chloride staining and autoradiography. There were no differences in the extent of the hypoperfused zone among the four groups. In both protocols 1 and 2 the ratio of the extent of myocardial necrosis to the extent of the hypoperfused zone was significantly smaller in the treated groups (56.7 +/- 6.7% [n = 8], p less than 0.01 and 72.3 +/- 5.3% [n = 6], p less than 0.05 for protocols 1 and 2, respectively) than in the control groups (100.7 +/- 6.0% [n = 7] and 95.2 +/- 4.3% [n = 5] for protocols I and II, respectively). Thus gallopamil administered early after coronary artery occlusion had beneficial effects on the ischemic myocardium, which were sustained for at least 24 hours after the onset of infarction.     

Three-dimensional mapping of spontaneous ventricular arrhythmias in a canine thrombotic coronary occlusion model

INTRODUCTION: Ventricular tachycardia (VT) and ventricular fibrillation (VF) induced by thrombotic coronary occlusion were mapped in three dimensions in ten dogs. METHODS AND RESULTS: Thrombotic occlusion was induced using a wire to deliver current to the proximal left circumflex artery (LCX). In nine dogs, nonsustained VT (NSVT) arose from numerous focal sites. Sustained VT was initiated in six dogs (VT group) by a focus near or in the ischemic region. VT was maintained by a focus in the ischemic border in three dogs and by macroreentry that involved both the ischemic and nonischemic regions in the other three dogs. In five dogs, VT degenerated into VF due to intramural reentry in different locations. Mean total activation time (AT), the time for activation to traverse the ventricles, for a sinus beat when LCX current was first applied was 40 +/- 4 msec. In the four dogs in which VT occurred 3 to 7 minutes after total occlusion, sinus AT increased to 98 to 146 msec just before VT. Sinus AT in the four dogs without VT was always <98 msec. Mean AT of the first ten cycles of VT was significantly longer in those VTs that degenerated into VF (169 +/- 29 msec) than in those that did not (81 +/- 12 msec). CONCLUSION: Thrombotic LCX occlusion induced NSVT in 90%, VT in 60%, and VF in 50% of dogs. Focal mechanisms caused most NSVTs and VT initiation. VT was maintained by a focus near or in the ischemic region or by macroreentry involving both the ischemic and nonischemic regions. AT identified animals in which VT occurred soon after LCX occlusion and in which VT progressed to VF.     

Acute coronary artery occlusion and ischemia-related ventricular tachycardia during catheter ablation in the right ventricular outflow tract

Coronary artery injury is a rare complication of catheter ablation in the right ventricular outflow tract (RVOT). Furthermore, acute myocardial ischemia usually causes polymorphic ventricular tachycardia (VT) or ventricular fibrillation. We herein describe a case in which catheter ablation for VT originating from the RVOT provoked ischemia-related VTs due to acute occlusion of the left anterior descending artery.     

心肌梗死48小时后反复持续性室性心动过速的治疗经验三例

1 病例资料 病例1:患者男性,70 岁,以"胸痛伴气短5 d"于2018 年1 月18 日入院. 患者于入院前 5 d 出现心前区痛,伴胸闷,持续数小时后自行缓解,未诊治;1 d 前胸闷加重,伴气短,夜间不能平卧,遂呼120来我院.既往慢性支气管炎病史20年,高血压病史30年,吸烟史50年.入院时呈端坐呼吸,心率91...     

Initiation of spontaneous ventricular tachycardia: from spark to fire

A famous restaurant is consumed by fire. As on‐lookers watch the blaze, the most frequently asked question is, “How did it start?” The more insightful question is posed by the firefighters, “Why did it burn?” Clearly, heat and flame were ever present in the kitchen. The spark itself was omni‐present, so the fire must result from some breakdown of the protective measures or changes in the flammable environment. This analogy applies to the relationship between PVC's and VT onset.     

Potential protective effect of high coronary wedge pressure on left ventricular function after coronary occlusion

To assess the potential of coronary collateral circulation to protect myocardium after occlusion of a coronary vessel, the mean coronary wedge pressure, the angiographic grade of collateral channels, and the left ventricular function were studied in 47 consecutive patients with mechanical recanalization of totally occluded coronary arteries. Coronary wedge pressure measurements were obtained 39 +/- 51 days (range, 2 hours to 361 days) after the presumed time of occlusion. The patients were divided into two groups: 31 with a coronary wedge pressure more than 30 mm Hg (group 1) and 16 with a coronary wedge pressure of or less than 30 mm Hg (group 2). Patients in group 1 had a significantly higher mean global left ventricular ejection fraction than those in group 2 (63 +/- 9% vs. 49 +/- 7%, p less than 0.001). Regional left ventricular function (artery-related area change) was also superior in group 1 compared with group 2 (47 +/- 11% vs. 36 +/- 10%, p less than 0.01). Global left ventricular function was significantly correlated to coronary wedge pressure (r = 0.51, p less than 0.001) but not to the angiographic presence of collaterals. The data suggest that a high coronary wedge pressure is associated with improved left ventricular function after coronary artery occlusion and that coronary wedge pressure more accurately reflects the physiological role of collaterals than their angiographic presence.     

Nitroglycerin-induced reduction in the incidence of spontaneous ventricular fibrillation during coronary occlusion in dogs

Previous investigations have demonstrated that nitroglycerin reduces ischemic injury and enhances ventricular electrical stability during coronary occlusion in dogs. These beneficial effects were potentiated by preventing drug-induced hypotension with alpha adrenergic agonists. To determine whether nltroglycerin can prevent spontaneous post-occlusion ventricular fibrillation, 27 open chest dogs were assigned in random fashion to two groups—control (saline infusion) and nitroglycerin-treated (0.45 mg intravenous bolus infusion followed by 0.3 mg/ min continuous infusion). After 10 minutes of infusion the left anterior descending and septal coronary arteries were occluded at their origins. Hypotensive effects of nitroglycerin were prevented by intermittent intravenous doses of methoxamine; mean arterial pressure and heart rate in control and treated animals were thus indistinguishable. Infusions continued until ventricular fibrillation occurred or 30 minutes elapsed. Twelve of 13 control dogs died with ventricular fibrillation; only 7 of 14 nitroglycerin-treated dogs died (P < 0.05). Thus, nitroglycerin may be capable of exerting important and unique beneficial effects in patients with acute myocardial infarction since, with its hypotensive effects obviated by alpha adrenergic agonists, it markedly diminishes ischemic injury, enhances ventricular electrical stability, and significantly reduces the incidence of spontaneous ventricular fibrillation in an experimental model of acute myocardial infarction.