Archive for the ‘Bradycardia’ Category


Evidence exists that SAM of the mitral valve begins even before aortic valve opening and onset of ejection. If this is so, increased inotropy after the long diastole certainly plays a greater role in the increased obstruction than can be appreciated with the methodology available to us. Present attempts at better delineating this pre-ejection component of the SAM before and during CSP are being pursued. However, again, this component (increased force of contraction) cannot explain per se the different responses to CSP in those with HOCM and those with AS, whereas the concept of decreased afterload and its different effects on an anatomically stenotic aortic valve and a dynamic LV tract obstruction can. (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Conclusion
  • 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. (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Outcome
  • Possible Mechanisms
    Transient and sudden slowing of the heart, by-applying CSP or by manipulating the pacing rate, may increase LV outflow obstruction by one or more of several mechanisms: Starling’s law, the Woodworth effect, or decreased afterload.
    First, based on Starling’s law of the heart, the long diastolic period could allow more complete LV filling (notwithstanding the marked stiffness of the hypertrophied myocardium) leading to increased fiber length and tension, which then enhance the force of contraction at the next systole. No tangible proof exists for this. Angiographic evidence suggests just the opposite, and no increase in septal-posterior wall diastolic dimension could be seen in any of our patients. (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Discussion
  • Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Aortic StenosisThe maximum instantaneous pressure gradient in the 21 patients was 41 ±25 mm Hg and the mean pressure gradient was 32±21 mm Hg. Heart rate decreased with CSP in all 21 patients; the Doppler velocity pattern and calculated pressure gradient and murmur intensity did not change in 18 (Fig 2, 4, B). The pressure gradient increased in only three patients (Fig 2) canadian health mall. The murmur intensity increased only in one of these three patients. The maximal instantaneous pressure gradient for the entire group increased to 44±28 mm Hg during CSP (p>0.05). (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Aortic Stenosis
  • Table 1 and Figure 2 show the maximum velocities and pressure gradients before and during CSP according to heart rate and echophonocardiographic responses. In the entire group of 30 patients, the mean pressure gradient increased by 33 ±29 mm Hg (median change, 28.6 mm Hg). In the subgroup of 24 patients in whom the murmur clearly increased, the mean pressure gradient increased from 41 ±30 mm Hg to 81±49 mm Hg (p<0.005).
    The continuous Doppler signal envelope configuration changed considerably in almost all cases, particularly when the baseline signal velocity had been relatively low (Fig 3, 4); in these cases, the signal pattern that had initially appeared almost normal became characteristic of subvalvular obstruction with the “knee” and concave leftward appearance that give the typical asymmetric contour to the velocity envelope in this disease. (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Results
  • Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: CSP: Effects on Heart Rate and MurmurWith the patient lying quietly in the left lateral decubitus position, gentle pressure was applied to the right carotid sinus during five or fewer cardiac cycles; pressure was subsequently applied to the left carotid sinus if pressure on the right did not slow the heart rate as monitored on the ECG Source antibiotics online. If necessary, firmer pressure or massage was then applied to the right carotid sinus. In all patients, heart rate was recorded; murmur intensity and characteristics were monitored with the stethoscope, recorded graphically on a commercially available phonocardiographic recorder, and graded on a six-point scale.
    Two patients with DDD pacemakers were similarly studied before and after the pacemaker rate w^as slowed transiently with an external pacemaker programmer; CSP was not applied. Three additional patients with HOCM who underwent diagnostic catheterization were subjected to atrial pacing faster than the sinus rate. Pacing was either slowed or stopped and simultaneous LV and aortic pressures were recorded; again, no CSP was applied. (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: CSP: Effects on Heart Rate and Murmur
  • Valvular AS was diagnosed by documenting a peak pressure gradient of at least 20 mm Hg by Doppler echocardiography across a stenotic aortic valve with or without calcification.
    Ultrasound imaging was performed with the Aloka SSD-870 or 860 systems, with 2.5- and 3.5-MHz transducers (Aloka Ltd; Tokyo, Japan). Assessment of myocardial hypertrophy was performed by M-mode echocardiography in the long- and short-axis parasternal planes. Localization of the site of increasing instantaneous velocity in the outflow tract was accomplished using a pulsed Doppler transducer. Localization of “aliasing” was obtained using the color Doppler mode of the SSD-870 system in the apical five-chamber view. (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Materials and Methods
  • 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
    (more…)

  • Comments Off on Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis
  • Categories


    Advertising


    Most Popular

    • None found

    Recent Comments

    • None found