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Influence of left ventricular hypertrophy on left ventricular function during dynamic exercise in the presence or
1First Department of Internal Medicine, Nagoya University Hospital, Japan.
Insights
Left ventricular hypertrophy (LVH) and coronary artery disease (CAD) independently raise cardiac filling pressures during exercise. Combining LVH and CAD severely impairs left ventricular function under stress.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Exercise Physiology
Background:
- Left ventricular hypertrophy (LVH) increases myocardial ischemia risk.
- Independent effects of LVH and coronary artery disease (CAD) on hemodynamics during exercise are not fully understood in humans.
Purpose of the Study:
- To investigate the impact of LVH, with or without CAD, on hemodynamic responses during exercise.
- To assess the independent and combined effects of LVH and CAD on cardiac function.
Main Methods:
- 78 patients underwent symptom-limited supine leg exercise tests.
- Patients were categorized into four groups: no LVH/CAD, LVH only, CAD only, and both LVH and CAD.
- Hemodynamic parameters, including pulmonary artery wedge pressure, were measured at rest and peak exercise.
Main Results:
- Pulmonary artery wedge pressure significantly increased during exercise in all groups compared to rest.
- LVH and CAD independently elevated peak pulmonary artery wedge pressure.
- A combination of LVH and CAD resulted in the highest pulmonary artery wedge pressure, indicating severe left ventricular dysfunction.
Conclusions:
- Both LVH and CAD are independent contributors to increased left ventricular filling pressures during exercise.
- The presence of both LVH and CAD leads to significant left ventricular dysfunction during physical exertion.
Objectives:
We investigated the influence of left ventricular hypertrophy in the presence or absence of coronary artery disease on hemodynamic characteristics during exercise in subjects without previous myocardial infarction.
Background:
Left ventricular hypertrophy has been found to increase the vulnerability of the myocardium to the development of ischemia. However, the independent influences of left ventricular hypertrophy and coronary artery disease have not been assessed in humans.
Methods:
Symptom-limited supine leg exercise tests were performed by 78 patients. They were classified into the following subgroups: no coronary artery disease or left ventricular hypertrophy (group I, n = 30), left ventricular hypertrophy only (group II, n = 12), coronary artery disease only (group III, n = 20) and both left ventricular hypertrophy and coronary artery disease (group IV, n = 16). Mean left ventricular mass index was 105, 158, 109 and 159 g/m2 in groups I to IV, respectively.
Results:
Pulmonary artery wedge pressure increased from 6 +/- 3 (mean +/- SD) mm Hg at rest to 10 +/- 5 mm Hg at peak exercise in group I, from 8 +/- 2 to 18 +/- 8 mm Hg in group II (p < 0.05 vs. group I), from 6 +/- 3 to 23 +/- 6 mm Hg in group III (p < 0.01 vs. group I) and from 8 +/- 4 to 30 +/- 7 mm Hg in group IV (p < 0.01 vs. group I; p < 0.01 vs. group II; p < 0.05 vs. group III). Multiple regression analysis showed that the number of diseased coronary vessels and left ventricular mass index were independent predictors of peak pulmonary artery wedge pressure (F = 59.2 and 19.1, respectively; multiple correlation coefficient r = 0.74, p < 0.0001).
Conclusions:
Left ventricular hypertrophy and coronary artery disease independently increased left ventricular filling pressure during supine leg exercise. Severe left ventricular dysfunction was induced by exercise when both conditions were present.