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Coronary haemodynamics in left ventricular hypertrophy
1Department of Medical Cardiology, Royal Infirmary, Glasgow.
Insights
Patients with left ventricular hypertrophy have reduced coronary blood flow, indicating an inadequate blood supply. This study found no upward shift in the autoregulation range during hypotension, despite observed electrocardiographic changes.
Area of Science:
- Cardiovascular Physiology
- Clinical Cardiology
- Hemodynamics
Background:
- Left ventricular hypertrophy (LVH) increases cardiovascular risks.
- LVH patients show ECG changes and dysfunction during hypotension.
- Previous research suggested an upward shift in autoregulation limits.
Purpose of the Study:
- To quantify coronary blood flow (velocity) and reserve during acute hypotension in LVH patients.
- To investigate the impact of hypotension on coronary hemodynamics in LVH.
Main Methods:
- Studied patients with LVH (hypertensive or atypical chest pain) and normal epicardial vessels.
- Measured left coronary blood flow velocity at rest and during hyperemia (adenosine) under induced hypotension (sodium nitroprusside).
- Assessed left ventricular mass via echocardiography and coronary blood flow using Doppler catheter and quantitative angiography.
Main Results:
- Coronary blood flow velocity was stable with physiological blood pressure but sensitive to pressure changes during maximal hyperemia.
- Absolute coronary blood flow, normalized for LV mass, was lower in hypertensive LVH patients at rest and during hyperemia.
- No upward shift in the lower limit of coronary autoregulation was detected.
Conclusions:
- Findings suggest an insufficient blood supply to the hypertrophied heart.
- The study did not support an upward shift in the autoregulatory range of coronary blood flow in LVH patients during hypotension.
Background:
Left ventricular hypertrophy is associated with an increased risk of cardiovascular morbidity and mortality. Previous studies have shown that patients with left ventricular hypertrophy develop electrocardiographic changes and left ventricular dysfunction during acute hypotension, and suggest that the lower end of autoregulation may be shifted upwards.
Aim:
To measure coronary blood flow (velocity) and flow reserve during acute hypotension in patients with left ventricular hypertrophy.
Patients:
Eight patients with atypical chest pain and seven with hypertensive left ventricular hypertrophy; all with angiographically normal epicardial vessels.
Setting:
Tertiary referral centre.
Methods:
The physiological range of blood pressure was determined by previous ambulatory monitoring. Left ventricular mass was determined by echocardiography. At cardiac catheterisation, left coronary blood flow velocity was measured using a Judkins style Doppler tipped catheter. During acute hypotension with sodium nitroprusside, coronary blood flow velocity was recorded at rest and during maximal hyperaemia induced by intracoronary injection of adenosine. Quantitative coronary angiography was performed manually.
Results:
For both groups coronary blood flow velocity remained relatively constant over a range of physiological diastolic blood pressures and showed a steep relation with diastolic blood pressure during maximal hyperaemia with intracoronary adenosine. Absolute coronary blood flow (calculated from quantitative angiographic data), standardised for left ventricular mass, showed reduced flow in the hypertensive group at rest and during maximal vasodilatation.
Conclusion:
The results are consistent with an inadequate blood supply to the hypertrophied heart, but no upward shift of the lower end of the autoregulatory range was observed.