Haruyuki Nakagawa

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.

Triggering mechanism for neurally mediated syncope induced by head-up tilt test: Role of catecholamines and response to propranolol

OBJECTIVES We studied the triggering mechanism for neurally mediated syncope. BACKGROUND Although increased transient sympathetic tone is thought to be necessary for the development of neurally mediated syncope, little is known about the triggering mechanism for neurally mediated syncope. METHODS Plasma epinephrine (EP) and norepinephrine (NE) levels were assessed in 20 syncope patients during tilt test (80 degrees, 15 min) with and without isoproterenol (ISP, 0.01, 0.02 microg/kg/min). If syncope occurred, propranolol (0.1 mg/kg) was injected. RESULTS Eight patients experienced syncope during tilting alone, and 9 patients required ISP for syncope. In the negative response without ISP, NE showed a small statistical 1.7-fold increase at end of tilting and EP did not change during tilting. When syncope occurred during tilting alone, a significant 11.7-fold increase in EP at syncope was registered concomitant with a small 2.5-fold increase in NE. When patients experienced syncope during tilting with ISP, a significant 5.0-fold increase in EP at syncope was registered concomitant with a small 1.7-fold increase in NE. In patients without ISP, propranolol did not interrupt syncope. In patients with ISP, six of eight receiving propranolol responded to tilting negatively. CONCLUSIONS An increase of NE levels may result in inhibition of syncope and an EP surge may be a triggering mechanism for neurally mediated syncope. Comparatively low levels of EP may be enough to induce syncope during tilting with ISP compared with tilting alone. Propranolol is not effective in patients without ISP, but it frequently inhibits syncope in patients with ISP. Propranolol (0.1 mg/kg) may be insufficient to block the actions of high levels of circulating EP.

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