S. Lele

Diastolic ventricular interaction in chronic heart failure

BACKGROUND Diastolic ventricular interaction describes a situation in which the volume of one ventricle is directly influenced by the volume of the other ventricle. Such interaction is normally negligible, but it is accentuated in circumstances associated with pulmonary hypertension and volume overload. When this interaction occurs, acute volume unloading results in a reduction in right ventricular end-diastolic volume, as expected, but left ventricular end-diastolic volume paradoxically increases. Since chronic heart failure is a volume-overloaded state associated with pulmonary hypertension, we hypothesised that this interaction may be clinically important in patients with heart failure. METHODS A radionuclide technique incorporating cardiac scintigraphy was used to measure the effect of acute volume unloading, achieved by 30 mm Hg lower-body suction, on right and left ventricular end-diastolic volumes in 21 patients with chronic heart failure and 12 healthy individuals (controls). FINDINGS In nine heart-failure patients, there was a paradoxical increase in left ventricular end-diastolic volume in association with an expected decrease in right ventricular end-diastolic volume during lower-body suction. This response was not seen in the control group. The mean change in left ventricular end-diastolic volume differed significantly between the heart-failure patients and controls (6 [SD 19] vs -19 [12] mL, p = 0.0003). However, the change in right ventricular end-diastolic volume was similar in the two groups (-18 [11] vs -20 [8]%. p = 0.70). Patients who increased left ventricular end-diastolic volume during lower-body suction had higher resting pulmonary arterial and pulmonary capillary wedge pressures than the remaining heart-failure patients. INTERPRETATION The response of nine patients in our study suggests diastolic ventricular interaction, which we believe could be common in patients with chronic heart failure. This finding is relevant to their management, since it emphasises the importance of venodilator therapy. The relation between stroke volume and left ventricular end-diastolic volume, by the Frank-Starting law of the heart, may explain why some patients with chronic heart failure paradoxically increase stroke volume when pulmonary capillary wedge pressure is lowered with vasodilators.

Exercise Capacity in Hypertrophic Cardiomyopathy Role of Stroke Volume Limitation, Heart Rate, and Diastolic Filling Characteristics

BACKGROUND We previously showed that exercise capacity in patients with hypertrophic cardiomyopathy (HCM) is related to peak exercise cardiac output. Cardiac output augmentation during exercise is normally dependent on heart rate (HR) response and stroke volume (SV) augmentation by increased left ventricular end-diastolic volume and/or increased contractility. We hypothesized that in contrast to normal subjects, peak exercise capacity in patients with HCM is determined by the diastolic filling characteristics of the left ventricle during exercise, which would in turn determine the degree to which SV is augmented, and that HR is a relatively unimportant determinant of peak exercise capacity. METHODS AND RESULTS Twenty-three patients with HCM underwent invasive hemodynamic evaluation and measurement of maximal oxygen consumption (VO2max) during erect treadmill exercise to assess the relative importance of changes in HR and SV in determining exercise capacity. Hemodynamic responses to erect and supine exercise were compared in 10 of these patients. In a separate group of 46 patients with HCM, the relation between VO2max and exercise diastolic filling indexes was assessed. Peak HR during erect exercise was 92 +/- 8% of predicted maximum. VO2max was 29.0 +/- 6.4 mL.kg-1.min-1 and was related significantly to peak exercise cardiac index and SV index (r = .71, P < .001 and r = .66, P = .001, respectively) but not to peak HR, HR deficit, or resting or peak pulmonary capillary wedge pressure. Peak cardiac output during erect exercise was not related to peak HR (r = .13, P = NS). When erect and supine exercise were compared, peak HR was lower in the supine position (153.3 +/- 19.9 beats per minute supine versus 172.0 +/- 17.6 beats per minute erect, P = .003), but peak exercise cardiac index was similar (7.9 +/- 2.6 L.min-1.m-2 supine versus 7.5 +/- 2.8 L.min-1.m-2 erect). Pulmonary capillary wedge pressure was higher at rest in the supine versus erect position (15.3 +/- 5.2 versus 8.1 +/- 6.1 mm Hg) but was not significantly higher at peak exercise in the supine versus erect position (28.5 +/- 8 versus 22.4 +/- 11.6 mm Hg erect, P = NS). In the separate group of 46 patients with HCM, VO2max was significantly inversely related to time to peak filling at peak exercise (r = -.60, P < .0001) but did not correlate with time to peak filling at rest, resting ejection fraction, peak filling rate, or peak exercise peak filling rate. CONCLUSIONS SV is the major determinant of peak exercise capacity in the erect position in patients with hypertrophic cardiomyopathy. This in turn is determined by the exercise left ventricular diastolic filling characteristics. HR augmentation does not appear to be a major determinant of peak cardiac output in the erect position.

Abnormal Forearm Vascular Responses During Dynamic Leg Exercise in Patients With Vasovagal Syncope

BACKGROUND We have reported previously that in some patients with normal hearts who present with exercise syncope, abnormal forearm vasodilation is seen during leg exercise and tilt table tests are positive. This suggests that exercise syncope may be a variant of vasovagal syncope. In this study we tested the hypothesis that there is loss of the normal forearm vasoconstrictor response during dynamic leg exercise in an unselected population of patients with classic vasovagal syncope. METHODS AND RESULTS We evaluated forearm vascular responses during maximal semierect cycle exercise in 28 consecutive patients with vasovagal syncope and compared them with 30 age-matched control subjects. We also evaluated blood pressure responses during erect treadmill exercise (Bruce protocol). While forearm vascular resistance at rest was similar in the patients with vasovagal syncope and the control group, forearm vascular resistance was markedly lower in the patients than in control subjects at peak exercise (85 +/- 54 versus 149 +/- 94 units, P = .002). Forearm vascular resistance fell by 3 +/- 48% during exercise in patients versus an increase of 135 +/- 103% in control subjects (P < .0001). Systolic blood pressure during erect exercise was lower in patients versus control subjects (155 +/- 32 versus 188 +/- 17 mm Hg, P < .0001). Six of the vasovagal patients complained of exercise syncope or presyncope on specific inquiry, and 4 of these 6 exhibited exercise hypotension during erect treadmill exercise testing. CONCLUSIONS Patients with vasovagal syncope exhibit a failure of the normal vasoconstrictor response in the forearm during dynamic leg exercise. Exercise syncope and presyncope are not uncommon in unselected patients with classic vasovagal syncope, as is exercise hypotension.

Mechanism of exercise hypotension in patients with ischemic heart disease. Role of neurocardiogenically mediated vasodilation.

BackgroundExercise-induced hypotension in patients with coronary artery disease (CAD) has been considered to be due to an inability to achieve an adequate increase in cardiac output to match the demands of exercise. We investigated 10 consecutive patients (9 men and 1 woman; age, 38 to 71 years; mean, 52 years) with angiographically documented CAD and exercise-induced hypotension (EIH) (BPPeak < BPRest). Ten approximately age- and sex-matched patients with documented CAD and normal exercise blood pressure response (NBP) served as control subjects. Methods and ResultsNine patients with EIH and all 10 control subjects underwent forearm plethysmography and radionuclide ventriculography (RNV) during semierect cycle exercise. Forearm vascular resistance (FVR) fell by 35 ± 21% in exercise-induced hypotension patients versus an increase of 78 ± 65% in patients with an NBP response (P < .0001). Left ventricular ejection fraction increased by 5.1 ± 7.5% in the group with EIH versus a fall of 4.1 ± 6.2% in the control group (P = .004). Cardiac output at peak exercise (RNV) increased by 2.2 ± 0.89-fold in the group with EIH versus 1.49 ± 0.47-fold in the control group (P = .04). The tenth patient in the group with EIH underwent invasive hemodynamic evaluation during erect exercise. Systolic blood pressure fell (136/80Rest to 50/40Peak) and cardiac output (Fick) tripled, whereas calculated systemic vascular resistance decreased by a factor of 10. Successful angioplasty to an isolated circumflex lesion resulted in resolution of symptoms and abnormal hemodynamic responses during exercise. ConclusionsAbnormal vasodilation associated with a normal or even increased rather than decreased cardiac output response appears to be an important mechanism underlying EIH in some patients with CAD. In the present study, this appears to have been the dominant mechanism in 8 and contributory in 2 of the consecutive patients studied.