Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: OutcomeWhatever combination of mechanisms is invoked to explain the increase in outflow obstruction in patients with HOCM has to explain why the increase does not occur in those with AS. The first two mechanisms evidently occur in both. What is it, then, that is unique to HOCM? We propose that the reduced afterload is indeed a major, if not the primary, cause for the increased obstruction, based 011 the theory that SAM of the mitral valve, due either to drag forces or to lift forces, contributes in a major way to the dynamic obstruction of HOCM. Transient and sudden cardiac slowing allows for more complete aortic decompression and abruptly reduces the afterload after the long pause; this facilitates LV emptying at the next systole and enhances initial blood flow velocity past the mitral leaflet (and lifts it more) or into it (and drags it more) into the outflow tract Source buy birth control online. This would probably play a much smaller role in the fixed obstruction of significant valvular aortic stenosis. Furthermore, a positive inotropic effect (the Woodworth effect) and whatever peripheral vasodilation may be induced by CSP would accentuate afterload reduction in HOCM but would exert little or no effect in AS. Starling’s law may also contribute to this fundamental mechanism. On the other hand, a vagally induced reduction in force of contraction could serve to modulate or even abolish the expected increase in obstruction, as may have been the case in two of our patients.
Finally, although mitral insufficiency undoubtedly contributes to the murmur of HOCM, it is unclear to what extent it contributes to the increase in the intensity of the murmur with CSP, since we were unable to document any substantial worsening of mitral regurgitation. It would appear that it is not necessary to invoke mitral insufficiency because the increase in outflow tract obstruction is sufficient to account for the increase in murmur intensity.
Study Limitations
Technical considerations in this clinical study did not allow us to define the relative impact of each of the above components on the LV obstruction seen after the long pause. Maximum change in pressure per unit of time was not measured because it is not totally independent of preload and because catheterization was performed with fluid-filled catheters and not with catheter-tip pressure transducers. Echocar-diographic indices of myocardial contractility, such as mean velocity of circumferential fiber shortening, also were not calculated because simple measurements of LV end-diastolic and end-systolic dimensions and the slope of posterior wall contraction were clearly not altered by CSP. Thus, this study does not prove unequivocally that contractility was actually enhanced. However, enough experimental evidence exists to accept this as a possible factor.