February 1, 1994European Heart Journal233 citations
View Full PaperInfluence of the force—frequency relationship on haemodynamics and left ventricular function in patients with non-failing hearts and in patients with dilated cardiomyopathy
Key Result
Right ventricular pacing at increasing rates increased cardiac index in non-failing hearts (2.9 to 3.5 L/min/m2; P<0.01) but decreased it in failing dilated cardiomyopathy (2.6 to 2.2 L/min/m2; P<0.05).
Structured PICO
Does increasing heart rate via right ventricular pacing affect haemodynamics and left ventricular function differently in patients with normal hearts versus those with dilated cardiomyopathy?
P
Population
17 patients, comprising 8 with normal left ventricular function and 9 with failing dilated cardiomyopathy (NYHA II-III), undergoing right ventricular pacing.
I
Intervention
Right ventricular pacing at increasing rates (100, 120, and 140 beats/min).
C
Comparator
Baseline pacing rate (slightly above sinus rate).
O
Outcome
Haemodynamic parameters including cardiac index, maximum rate of left ventricular pressure rise, ejection fraction, and left ventricular volumes/pressures.surrogate
This study demonstrates in vivo that the force-frequency relationship is positive in non-failing human hearts but negative in failing hearts with dilated cardiomyopathy, confirming prior in vitro experimental findings.
Abstract
In isolated human myocardium it was shown that a positive force-frequency relationship occurs in non-failing myocardium; however, the force-frequency relationship was found to be inverse in myocardium from failing human hearts. In order to investigate the clinical relevance of these experimental findings, the influence of heart rate changes on haemodynamics and left ventricular function was studied in eight patients without heart failure and in nine with failing dilated cardiomyopathy (NYHA II–III). Right ventricular pacing was performed at a rate slightly above sinus rate and at 100, 120 and 140 beats. min−1 Haemodynamic parameters were obtained by right heart catheterization and by high-fidelity left ventricular pressure measurements. Left ventricular angiography was performed at basal pacing rate and at 100 and 140 beats. min−1 With increasing heart rate, cardiac index increased in patients with normal left ventricular function from 2·9 ± 0·2 to 3·5 ± 0·21. min−1. m−2 (P<0·01) and decreased continuously in patients with dilated cardiornyopathy from 2·6 ± 0·1 to 2·2 ± 0·11. min−1 . m−2 (P<0·05). With increasing heart rate, the maximum rate of left ventricular pressure rise increased in non-failing hearts from 1388 ± 86 to 1671 ± 88 mmHg. s−1 (P<0·01) and did not change in failing hearts. Ejection fraction decreased from 27 ± 3% to 19 ± 2% in patients with dilated cardiomyopathy (P<0·05) when the pacing rate was changed from 84 ± 2 beats. min−1 to 140 beats. min−1, which was associated with a significantly increase in end-systolic volume without significantly changes in end-diastolic volume. In patients with normal left ventricular function, when the pacing rate was changed from 85 ± 3 beats. min−1 to 140 beats. min−1, end-diastolic volume decreased significantly by 13%, whereas left ventricular end-systolic volume and ejection fraction did not significantly change. Left ventricular systolic and end-diastolic pressures did not significantly change with pacing tachycardia in either group. The frequency-related changes in left ventricular volumes and pressures indicate that the differrent haemodynamic effects of pacing tachycardia in both groups of patients result predominantly from frequency effects on myocardial function and not from frequency effects on preload or afterload. These data indicate that recent experimental findings of positive force-frequency effects in non-failing and negative force-frequency effects in failing human myocardium are relevant for the intact heart.