Takao Baba

Prolonged Paced QRS Duration as a Predictor for Congestive Heart Failure in Patients with Right Ventricular Apical Pacing

Background: The recent studies showed that right ventricular (RV) pacing was associated with worsening of heart failure. The aim of this study is to clarify the clinical significance of paced QRS duration during RV pacing to predict congestive heart failure (CHF) patients.

Sustained Left Ventricular Tachycardia Terminated by Dipyridamole: Cyclic AMPMediated Triggered Activity as a Possible Mechanism

Sustained VT in two patients was terminated by intravenous administration of dipyridamole, an adenosine transport inhibitor. VT was induced by rapid atrial or ventricular pacing, isoproterenol, or dibutyryl cyclic AMP infusion, or exercise. VT also was aborted by adenosine triphosphate or acetylcholine injection, or by vagal stimulation. VT was terminated or prevented by verapamil or propranolol. In addition, arrhythmias were prevented by oral administration of dipyridamole. These results suggest that VT is due to cyclic AMP‐mediated triggered activity and that inhibition by dipyridamole may be due to a reduction in the intracellular concentration of cyclic AMP.

Effects of nicorandil, a potassium channel opener, on idiopathic ventricular tachycardia.

OBJECTIVES We assessed the effects of the adenosine triphosphate (ATP)-sensitive potassium channel opener, nicorandil, on ATP- and verapamil-responsive ventricular tachycardias (VTs). BACKGROUND Adenosine- or ATP-sensitive VTs are thought to be due to a nonreentrant mechanism, presumably delayed afterdepolarization. We suggest that this potassium channel opener may suppress ATP- and verapamil-sensitive VTs. METHOD The subjects included 13 patients with idiopathic VTs, 7 of whom had sustained VT and 6 of whom had nonsustained VT. We evaluated the effects of ATP, nicorandil and verapamil on VTs. RESULTS Sustained VT: Verapamil had preventive effects on seven VTs. Four VTs were terminated by ATP, and of these, nicorandil terminated two and prevented exercise-induced VT in the two others. Three ATP-insensitive VTs, which were determined to be due to a reentry by an electrophysiologic study, were not terminated by nicorandil. Nonsustained VT: All six VTs were inhibited by ATP, and five of these were suppressed by nicorandil. Verapamil inhibited four of the five VTs. QT intervals and the corrected QT intervals were significantly shortened by nicorandil. CONCLUSIONS Nicorandil suppresses ATP- and verapamil-responsive VTs. One of the mechanisms of suppression by nicorandil might be related to a reduction of calcium in the myocardium, because it reduces the action potential duration.

Onset heart rate and microvolt t-wave alternans during atrial pacing.

patient subgroup based on our a priori suspicion that these patients would benefit from an ICD and based on their high risk for death. These data, however, suggest that patients with severe heart failure should be considered for randomized trials, similar to patients with functional class II and III congestive heart failure. This risk for death may be reduced similarly in the functional class IV heart failure patients, but these patients, especially those with a history of ventricular arrhythmias, will remain a high-risk group, and will continue to be at risk for several forms of sudden death, including bradyarrhythmic and tachyarrhythmic death. It is possible that some patients did benefit from the ICD based on its backup bradycardia pacing capabilities. Although this cannot be excluded, it could still indicate the potential benefits of the ICD. These data indicate that early death is not inevitable in patients with functional class IV heart failure with malignant ventricular arrhythmias and an ICD implant. Important selection biases cannot be excluded. Patients who appeared to stabilize on medical therapy were more likely to be included. Exclusion of patients with functional class IV heart failure from future arrhythmia trials should be reconsidered.

Clinical, electrophysiological, and histopathological observations in supraventricular tachycardia.

Fifty patients with supra ventricular tachycardia (SVT) underwent clinical electrophysiological studies (EPS), endomyocardial biopsies und cardiac catheterizations. EPS revealed AV nodal reentrant tachycardia (AVNRT) in seven patients, AV reentrant tachycardia utilizing concealed AV bypass tracts (AVR‐ CBT) in nine patients, AV reentrant tacycardia utilizing AV bypass tracts with ventricular preexcitation (manifest WPW) in 13 patients, sinus nodal or intra‐atrial reentrant tachycardia (SNRT or TART) in three patients, atrial flutter (AF) in nine patients, automatic atrial tachycardia (AAT) in jive patients, and multifocal atrial tachycardia (MAT) in four patients. According to the clinical observations, three patients with AVNRT (43%), six with AVH‐CBT (67%), six with manifest WPW (46%), two with SNRT or IART (67%), eight with AF (89%), two with AAT (40%), and two with MAT (50%) showed other accompanying clinical abnormalities. In all patients who were studied histologically, changes in the myocardium were seen; myocarditic changes, postmyocarditic changes and nonspecific abnormalities were present in six (12%). 15 (30%), and nine (18%) respectively. Myocardial changes were observed in four out of seven cases with AVNRT (57%), in six out of nine with AVR‐CBT (67%), in five out of 13 with manifest WPW (38%), in two out of three with SNRT or IART (67%), in six out of nine with AF (67%), in all five cases of AAT (100%), and in two out of four with MAT (50%). Nineteen out of 32 without clinical abnormalities except for arrhythmias (59%) had myocardial changes (six had myocarditic changes, ten had postmyocarditic changes, and three had nonspecific abnormalities). On the other hand, nine out of 21 with myocarditic or postmyocarditic changes were accompanied with various arrhythmias other than SVT (two had SSS, five had AV block or rBBB, and two had VT). Elevated LVEDP was present in 36% of the group with normal myocardium and in 53% of the group with myocardial changes. However, the low EF was shown in no patients with normal myocardium but in 21% of the group with myocardial changes. The low CI was also shown in only 9% of the group with normal myocardium but in 28% of the group with myocardial changes. These results suggest that patients with SVT may exhibit several histopathological changes in the myocardium, even in the absence of any clinical organic heart disease.

Hypersensitivity of cerebral artery response to catecholamine in patients with neurally mediated syncope induced by isoproterenol.

N mediated syncope is a frequent cause of syncope not resulting from organic dysfunction.1 The head-up tilt test (HUT) is useful for diagnosing syncope and investigating the pathophysiologic mechanisms involved in this syndrome.1–3 Cerebral circulation during syncope has been largely unexplored. We studied cerebral circulation during the HUT by measurement of cerebral blood flow velocity (CBFV) using transcranial Doppler ultrasonography that has emerged as a reliable technique for assessing both blood flow and cerebral vasoreactivity.4,5 • • • The subjects were 10 patients (6 men and 4 women, aged 33 6 15 years) with a history of recurrent syncope of unknown origin (Table I). The HUT was performed in the fasting state. All cardioactive medications were discontinued at least 3 days before the study. Subjects were connected to a standard electrocardiographic monitor for continuous evaluation of heart rate and rhythm. Blood flow velocity of the middle cerebral artery was monitored at a mean depth of 55 mm via the transtemporal approach with a 2-MHz pulsed-wave transcranial Doppler apparatus (LOGIQ 500 MD, GE Yokogawa Medical Systems Inc., Tokyo, Japan). Transcranial Doppler sonography was used to assess CBFV (cm/s) in the middle cerebral artery during the HUT as frequently as possible with the following indexes: systolic, diastolic, and mean velocity. Gosling’s pulsatility index ([(systolic velocity) 2 (diastolic velocity)]/mean velocity) and resistance index ([(systolic velocity) 2 (diastolic velocity)]/systolic velocity) in the supine position and on presyncope were obtained, and the rate of change (D[(presyncope/supine position) 2 1] 3 100) was calculated. In the HUT, the subject was positioned at an angle 180° from the horizontal position on a tilt table until syncope was induced or for a maximum of 30 minutes. If syncope did not occur during the HUT, the subject was lowered to the horizontal position for 10 minutes, and isoproterenol (0.01, 0.02 mg/kg/min) was administered intravenously according to our previous report.6 The HUT was then continued as before for 15 minutes. Values of CBFV and pulsatility and resistance indexes were compared using the paired t test to determine if CBFV changed significantly during the HUT. All results are expressed as mean 6 SD, and a p value ,0.05 was considered statistically significant. None of the subjects had structural heart disease or a cerebral disease as assessed with a conventional, noninvasive evaluation. Syncope occurred in 5 of 10 subjects. One subject (no. 1) experienced syncope with the HUT alone. Four subjects experienced syncope by the HUT with isoproterenol provocation. Only subject 5 (among the 4 subjects) experienced syncope without hypotension and bradycardia (Table II). In 4 of 5 subjects with induced syncope, blood pressure and all CBFV indexes decreased, and pulsatility and resistance indexes increased with presyncope. In the remaining subject (no. 5) with induced syncope, pulsatility and resistance indexes and CBFV decreased without hypotension. On the other hand, syncope did not occur in 5 of 10 subjects. Blood pressure, heart rate, systolic velocity, mean velocity, and pulsatility and resistance indexes increased when subjects were in the supine and upright positions with and without isoproterenol provocation. Only the change in heart rate was significant. In the upright position, pulsatility and resistance indexes increased when blood pressure increased and these decreased when blood pressure decreased. This occurred with and without isoproterenol provocation. In 4 of 5 subjects with induced syncope using isoproterenol provocation, systolic velocity and pulFrom the Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan. Dr. Kobayashi’s address is: 142– 8600, 1–5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan. Manuscript received June 28, 1999; revised manuscript received and accepted December 20, 1999. TABLE I Response to Head-Up Tilt Test