Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic StenosisThe systolic ejection murmur of hypertrophic obstructive cardiomyopathy (HOCM) increases in intensity in about 80% of patients if and when carotid sinus pressure (CSP) succeeds in slowing the heart rate. This does not generally occur in patients with valvular aortic stenosis (AS). We hypothesized that this difference in response reflects increased left ventricular (LV) outflow obstruction in HOCM that is not seen in AS, and that Doppler echocardiography would provide an excellent noninvasive modality to test this hypothesis in a reasonably large group of patients. Furthermore, we attempted to test whether it was the abrupt bradycardia or the CSP that was responsible for the effect. This Doppler echocardiography study was therefore undertaken to more clearly define the relationship of the induced bradycardia to LV outflow obstruction in HOCM, in which the obstruction is dynamic in nature, and in AS, in which the obstruction is anatomically fixed. In addition, another two patients with sequential atrioventricular (DDD) pacemakers and HOCM were studied before and after slowing of the pacemaker rate without CSP, and three patients were studied during and after slowing or cessation of atrial pacing at catheterization without CSP. cialis professional 20 mg

Materials and Methods
Patients
Thirty-six HOCM patients (25 men, 11 women; aged 52 to 80 years, mean age [±SD] was 65±9 years) and 21 AS patients (14 men, 7 women; aged 25 to 79 years, mean age wras 59 ±14 years) were studied. Of these, 12 HOCM patients and five AS patients had been studied previously. None had clinical evidence of carotid artery disease. None received p-blockers or calcium-channel blockers at the time of study. All gave informed consent after the goal of the study was explained to them. The local institutional human research review committee approved the research protocol.
HOCM was diagnosed by standard eehocardiographic criteria: (1) asymmetric or concentric ventricular hypertrophy; (2) systolic anterior motion (SAM) of the mitral valve in the left parasternal long-axis view and a distinct everting motion of the tip of the mitral leaflet(s) into the outflow tract in the apical five-chamber view; and (3) the presence of increased maximal outflow velocity (>1.5 m/sec) and of the distinctive Doppler signal pattern on continuous Doppler interrogation of the outflow tract, either at rest or after provocative maneuvers.