Polymorphous ventricular tachycardia associated with acute myocardial infarction

BACKGROUND. During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). METHODS AND RESULTS. Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. CONCLUSIONS. Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.     

Inducible sustained ventricular tachycardia 4 years after experimental canine myocardial infarction: electrophysiologic and anatomic comparisons with early healed infarcts

We studied a group of 17 dogs 4 to 6 years after infarction produced by 2 hr occlusion of the anterior descending coronary artery followed by reperfusion. Dogs in this "late" infarct group were compared with a group of 24 dogs with "early" healed infarcts (2 to 24 weeks old). With signal-averaging techniques body surface potentials were recorded during sinus rhythm. After thoracotomy epicardial electrograms were recorded from 45 standardized sites within the infarcted region and characteristics of selected electrograms were compared with anatomic features of underlying myocardium. Epicardial recordings from the late infarct group demonstrated earlier local activation (p less than .001) and shorter electrogram duration (p less than .001) when compared with recordings from the early infarct group. There was less temporal dispersion of activation and electrogram duration among the 45 sites in dogs with late infarcts as measured by respective coefficients of variance (p = .007 and less than .001). With programmed stimulation six dogs in the late and eight in the early infarct group exhibited inducible sustained ventricular tachycardia. Mean cycle length of the tachycardia in dogs with late infarcts was significantly shorter (p = .035). Late potentials were notably less prominent in dogs in the late infarct group with ventricular tachycardia than in dogs in the early infarct group. Fewer abnormal electrophysiologic characteristics of late infarcts coincided with relatively less scar in the underlying myocardium. Moreover, the strength of electrophysiologic-anatomic correlations differed in late as opposed to early infarcts. The latter findings suggest long-term evolution of infarct anatomy. We conclude that a substrate for reentrant tachycardia is present in dogs 4 to 6 years after reperfused infarction. Conduction characteristics are less abnormal in these late healed infarcts and are associated with a shorter ventricular tachycardia cycle length and less pronounced late potentials on the body surface.     

Right ventricular myocardial infarction: From pathophysiology to prognosis

Right ventricle myocardial infarctions (RVMIs) accompany inferior wall ischemia in up to one-half of cases. The clinical sequelae of RVMIs vary from no hemodynamic compromise to severe hypotension and cardiogenic shock. Diagnosis is based on physical examination, electrocardiography, echocardiography and coronary angiography. Because the standard 12-lead electrocardiogram is insufficient for the assessment of RV involvement, right-sided precordial leads should always be included. Adequate fluid administration in combination with positive inotropic agents and early coronary reperfusion are crucial components of treatment, while diuretics and nitrates should be avoided. Intra-aortic balloon counterpulsation and right ventricle assist devices may be used with success in RVMIs associated with medically refractory heart failure. Right ventricular involvement appears to be an independent prognostic factor that dramatically increases in-hospital mortality, due, in part, to a significantly higher risk of hemodynamically compromising arrhythmias. Thus, using right-sided precordial leads and early RVMI identification to trigger an appropriately aggressive treatment protocol may improve patients’ prognosis.     

Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction

Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 +/- 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean follow-up of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated with mortality included: (1) treatment before 1981 (p less than 0.01); (2) anterior AMI (p less than 0.05); (3) short time from AMI to first episode of VT (p less than 0.06); and (4) multivessel coronary artery disease (p less than 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p less than 0.01); (2) greater than or equal to 3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p less than 0.05); and (4) anterior AMI (p less than 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p less than 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormalities of endocardial activation pattern in patients with previous healed myocardial infarction and ventricular tachycardia

Endocardial catheter mapping was performed in 27 patients with anterior wall acute myocardial infarction (AMI) and in 10 patients with inferior wall AMI. All patients had a history of ventricular tachycardia. Left ventricular breakthrough occurred at 10 +/- 4 ms after the QRS complex in inferior AMI and 11 +/- 7 ms after the QRS complex in anterior AMI. Total electrical activity recorded during sinus rhythm was 164 +/- 46 ms in inferior and 144 +/- 28 ms in anterior AMI (p = 0.05). Nine of the 10 patients with inferior AMI had complete activation of the anterior wall within the initial one-half of the QRS complex, compared with only 15 of the 27 patients with anterior AMI (p = 0.05). All 10 patients with inferior AMI had activation of the ventricular septum within the initial half of the QRS complex compared with only 13 of 27 with anterior AMI (p less than 0.005). None of the patients with inferior AMI had activation of the inferoposterior base within the initial one-half of the QRS complex, compared with 21 of 27 patients with anterior AMI (p less than 0.001). Complete activation of the anterior wall occurred at 33 +/- 15 ms in inferior and 58 +/- 30 ms in anterior AMI (p less than 0.005). Complete activation of the septum occurred at 38 +/- 12 ms in inferior and 63 +/- 28 ms in anterior AMI (p less than 0.005). Complete activation of the inferoposterior base occurred at 100 +/- 38 ms in inferior and 50 +/- 21 ms in anterior AMI (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

经皮穿刺心外膜电-解剖标测及射频消融心肌梗死后室性心动过速的实验研究

目的探讨经心外膜途径在电-解剖标测系统指导下行射频消融治疗心肌梗死后室性心动过速的可行性和安全性。方法成年中华小型猪共7只,采用经皮穿刺的方法将球囊置于左前降支中下部,封堵150 min建立心肌梗死模型。3～5周后将心肌梗死模型猪,行电生理检查诱发室性心动过速。经胸穿刺进入心包腔,采用电-解剖标测系统在窦性心律下进行心外膜电压标测和线性消融。射频消融后再次行电生理检查,不能再诱发室性心动过速为消融成功。结果存活的心肌梗死模型的猪7只,3～5周后行电生理检查,共诱发出单形性室性心动过速共8种,7种表现为右束支阻滞图形,1种表现为左束支阻滞图形,室性心动过速(VT)周长平均在(338±66)ms。1只猪同时诱发心室颤动,电除颤转复窦性心律。7只猪心包穿刺均成功,完成心外膜电压标测,沿瘢痕区到二尖瓣环或正常心肌区逐点进行线性消融。射频消融后再次行电生理检查,6只猪不能再诱发室性心动过速。结论经胸穿刺进入心包腔行心外膜标测和消融治疗心肌梗死后室速的方法是安全可行的,心外膜标测消融心肌梗死后室速的方法可以作为心内膜消融的一种有效补充方法。     

Exercise-induced ventricular arrhythmias in patients with healed myocardial infarction

Background: Controversy exists about the clinical and prognostic significance of exercise-induced ventricular arrhythmias late after myocardial infarction. The aim of the study was to identify the main clinical and prognostic features of exercise-induced ventricular arrhythmias in out-patients with healed Q-wave myocardial infarction. Methods: The study population was 777 consecutive patients who underwent a symptom-limited (Bruce protocol) treadmill test from May 1988 to January 1991 after myocardial infarction (at least 1 year). Clinical and exercise data were prospectively entered in a computerized database and retrospectively two different groups were selected: (1) 228 patients with exercise-induced ventricular arrhythmias; (2) 549 patients without. Incidence and morphology of exercise-induced ventricular arrhythmias, various exercise parameters and a follow-up were evaluated. Results: Patients with exercise-induced ventricular arrhythmias were older (P < 0.001), had higher blood pressure (P < 0.03) and peak exercise rate pressure product (P < 0.00) than the others. No difference was found in the incidence of exercise-ischaemia: either symptomatic or not. When simple (≤2 Lown) versus complex (≥3 Lown) exercise-induced ventricular arrhythmias were considered, the latter were more frequent in patients with anterior myocardial infarction, shorter exercise duration (P < 0.001) and lower exercise rate pressure product, lower ejection fraction and lower incidence of exercise-induced ischaemia. In the follow-up (mean 24 ± 13 month) there were 24 deaths: five (2.2%) in patients with exercise-induced ventricular arrhythmias and 19 (3.4%) in patients without. Cardiac event rate was similar in both groups. Conclusions: We conclude that in out-patients with healed myocardial infarction exercise-induced ventricular arrhythmias are quite frequent, but they are not associated with exercise-induced ischaemia, either symptomatic or not. Exercise-induced ventricular arrhythmias seem to be related to age or peak workload. Moreover patients with these arrhythmias have no adjunctive negative risk on prognosis.     

Gitelman's syndrome with exercise-induced ventricular tachycardia.

A 62-year-old female with palpitations was admitted to hospital where she recorded 12,299 monofocal ventricular premature contractions (VPCs) in 24 h and nonsustained ventricular tachycardia (VT) on exertion. She had hypokalemia with renal potassium wasting, a chloride-resistant metabolic alkalosis, elevated plasma renin, elevated plasma aldosterone (relative to the serum K concentration), hypomagnesemia with renal magnesium wasting, decreased urine calcium excretion, and normal blood pressure. The hypokalemia and hypomagnesemia were thought to have precipitated the VT. The coronary angiogram showed normal coronary arteries; however, the left ventriculogram revealed akinesis of the posterolateral wall. Because the VT could not be induced by programmed electrical stimulation either before or during intravenous administration of isoproterenol, the VPC with the same QRS morphology as the VT became the target of radiofrequency catheter ablation (RF-CA). Intracardiac mapping showed that the earliest activation site was situated in the asynergic area of the left ventricle (LV) and radiofrequency catheter ablation directed at the LV asynergy area completely eliminated the VPCs without any complications. During the follow-up period (6 months), she was free from palpitation and VT was not clinically documented.     

Reproducibility of exercise-induced ventricular arrhythmia after myocardial infarction.

To evaluate the reproducibility of exercise-induced ventricular arrhythmia, 155 men with a mean age of 53 +/- 8 years underwent serial exercise testing 3 to 52 weeks after myocardial infarction. The reproducibility of categorical test responses, that is, the presence or absence of ventricular arrhythmia, was evaluated with the kappa coefficient, which considers negative as well as possible test responses and expresses reproducibility above the chance level. Reproducibility was highest at an intertest interval of 1 to 5 days and was not enhanced by further categorizing premature ventricular complexes as simple or complex based on their frequency or configuration. Continuous response measures such as frequency of premature ventricular complexes yielded higher reproducibility than categorical responses. Continuous response measures appear preferable to categorical responses for evaluating the clinical significance and response to antiarrhythmic therapy of ventricular arrhythmias.     

Incidence of acute myocardial infarction in patients with exercise-induced silent myocardial ischemia

Fifty-five patients with angiographically proved coronary artery disease (CAD) underwent Bruce protocol exercise stress testing with thallium-201 imaging. Twenty-seven patients (group I) showed myocardial hypoperfusion without angina pectoris during stress, which normalized at rest, and 28 patients (group II) had a similar pattern of reversible myocardial hypoperfusion but also had angina during stress. Patients were followed for at least 30 months. Six patients in group I had an acute myocardial infarction (AMI), 3 of whom died, and only 1 patient in group II had an AMI (p = 0.05), and did not die. Silent myocardial ischemia uncovered during exercise stress thallium testing may predispose to subsequent AMI. The presence of silent myocardial ischemia identified in this manner is of prognostic value, independent of angiographic variables such as extent of CAD and left ventricular ejection fraction.     

急性心肌梗死非持续和持续室性心动过速的Q—T离散度

为研究急眭心肌梗死伴持续和非持续室性心动过速患者间Q-T离散度和其它心电图参数之间的关系。比较14例急性心肌梗死伴持续室性心动过速和26例伴非持续室性心动过速患者的心室Q-T离散度、Q-T和Q-T_c间期。结果显示持续和非持续室性心动过速患者之间的Q-T离散度以及相邻胸导联Q-T离散度差异有显著意义(110.1±7.80对80.8±4.4,105.9±6.9对67.6±4.0,P<0.01)。我们认为相邻导联Q-T离散度增大极易出现室性心动过速,Q-T离散度大于110ms有发生持续室性心动过速的危险。而Q-T离散度在80—110ms之间有非持续室性心动过速的可能性。     

Verapamil-sensitive left anterior fascicular ventricular tachycardia associated with a healed myocardial infarction: changes in the delayed Purkinje potential during sinus rhythm

Uncommon association of left anterior fascicular ventricular tachycardia (VT) with a healed myocardial infarction (MI) is described. A 55-year-old man with a history of anteroseptal MI had verapamil-sensitive VT. The VT exhibited a right bundle branch block configuration and right-axis deviation. The VT exit was located at the left ventricular anterolateral wall. At the mid-anterior left ventricular septum, delayed Purkinje potentials were seen during sinus rhythm, and the optimal pace map was obtained with pace delay. During the VT, diastolic and systolic Purkinje potentials were simultaneously recorded at the same site. Ablation targeting the delayed potentials during sinus rhythm prolonged the time between QRS onset and the delayed potentials, and the VT no longer became inducible when the delayed potentials were completely eliminated. Left anterior fascicular VT develops in post-MI patients; ischemia-injured His-Purkinje system may be involved in the mechanism of the VT.