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systolic flow augmentation in hearts ejecting into a model of stiff aging vasculature. Influence on myocardial
1Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21287.
Insights
Arterial stiffening increases cardiac workload but does not compromise myocardial blood flow. Enhanced pulsatility in stiff arteries may augment coronary perfusion, challenging previous assumptions about aging hearts.
Area of Science:
- Cardiovascular Physiology
- Biomedical Engineering
- Gerontology
Background:
- Age-related arterial stiffening increases ventricular systolic wall stress and widens pulse pressure.
- Reduced diastolic coronary perfusion pressure due to stiff arteries may impair myocardial oxygen supply-demand balance.
- Previous hypotheses suggest these vascular changes adversely affect the heart's workload and blood supply relationship.
Purpose of the Study:
- To test the hypothesis that age-related arterial stiffening adversely alters myocardial workload and blood supply.
- To investigate the impact of increased arterial pulse pressure on coronary perfusion and myocardial oxygen consumption.
- To examine the relationship between cardiac workload, coronary blood flow, and arterial pulsatility.
Main Methods:
- Surgically bypassed the native compliant aorta with a stiff tube in anesthetized dogs.
- Directed ventricular outflow into either the native aorta or the stiff bypass to alter arterial pulse pressure.
- Assessed cardiac workload using pressure-volume area (PVA) and myocardial oxygen consumption (MVO2).
- Measured regional and global coronary blood flow using the left anterior descending artery and microspheres.
- Evaluated myocardial supply-demand balance by comparing flow at matched workload and analyzing flow-PVA relations.
Main Results:
- Directing flow into the stiff bypass significantly increased arterial pulse pressure and ventricular systolic wall stress.
- Despite reduced diastolic perfusion pressure, mean coronary blood flow increased by 34% and maintained endocardial-to-epicardial flow ratios.
- Enhanced systolic perfusion contributed significantly to coronary flow augmentation, nearly equaling diastolic flow.
- Flow augmentation persisted at matched workloads and across a range of cardiac work loads.
Conclusions:
- Cardiac coupling with a stiff arterial system does not necessarily compromise myocardial flow relative to metabolic demand.
- Increased arterial pulsatility, particularly enhanced systolic perfusion, plays a crucial role in maintaining coronary perfusion under stiff arterial conditions.
- The findings suggest that enhanced arterial waveform pulsatility may actively augment coronary perfusion, challenging traditional views on arterial aging and cardiac function.
Abstract:
Age-related arterial stiffening and widening of the pulse pressure elevates ventricular systolic wall stress while it lowers diastolic coronary perfusion pressure. These changes are thought to adversely alter the balance between myocardial work load and blood supply. To test this hypothesis, the native compliant thoracic aorta was surgically bypassed by a stiff tube in reflex-blocked anesthetized dogs. Ventricular outflow was directed into either native aorta or the bypass; the latter resulting in an increase in arterial pulse pressure from 37.8 to 107.5 mm Hg (P < .001), with minimal change in mean pressure and flow. Cardiac work load was assessed by pressure-volume area (PVA), which combines external and internal left ventricular work and is linearly related to myocardial oxygen consumption (MVO2), and by MVO2 itself. Regional phasic and mean coronary flow were measured in the left anterior descending coronary artery, and global flow was assessed by radiolabeled microspheres. Myocardial supply-demand balance was assessed by comparing flow at matched PVA or MVO2, flow-PVA relations, and endocardial-to-epicardial flow ratios. When blood flow was directed into the stiff bypass tube, peak systolic pressure, wall stress, and PVA all rose nearly 50%, yet diastolic perfusion pressure fell by 20 mm Hg (all P < .01). Rather than being compromised, however, mean coronary flow rose by 34%, maintaining the same endocardial-to-epicardial flow ratio (approximately 1.1). Flow augmentation persisted when data were compared at matched work load (PVA or MVO2), and mean arterial pressure, as well as over a range of work loads (P < .001 from ANCOVA of flow-PVA relations). The increased flow resulted from enhanced systolic perfusion, which nearly equaled diastolic flow when ejection passed into the stiff bypass. These data counter the notion that cardiac coupling with a stiff arterial system (as with aging) necessarily compromises myocardial flow versus metabolic demand. However, the data highlight a greater role of systolic flow under such conditions and also raise the novel suggestion that enhanced pulsatility of the arterial pressure waveform may itself augment coronary perfusion.