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Coronary vasodilator reserve is impaired in patients with hypertrophic cardiomyopathy and left ventricular
R Lorenzoni1, R Gistri, F Cecchi
1MRC Clinical Sciences Centre and Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Insights
Reduced blood flow to the heart muscle (myocardium) may cause systolic dysfunction in hypertrophic cardiomyopathy (HCM). Impaired coronary vasodilator capacity is linked to this dysfunction.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart condition.
- Systolic dysfunction is a common complication in HCM patients.
- The role of reduced myocardial blood flow in HCM-related systolic dysfunction is under investigation.
Purpose of the Study:
- To test the hypothesis that reduced myocardial blood flow contributes to systolic dysfunction in HCM.
- To investigate the relationship between coronary vasodilator reserve and systolic function in HCM patients.
Main Methods:
- Eighty-four patients with HCM underwent 2-dimensional echocardiography to assess left ventricular dimensions and fractional shortening.
- Myocardial blood flow (MBF) was measured using positron emission tomography (PET) with N13-ammonia or O15-water at baseline and after dipyridamole administration.
- Coronary vasodilator reserve (CVR) was calculated as the ratio of post-dipyridamole to baseline MBF.
Main Results:
- Patients in advanced NYHA classes exhibited significantly lower dipyridamole MBF and CVR.
- A positive linear correlation was found between fractional shortening and dipyridamole MBF.
- Patients with abnormal fractional shortening demonstrated significantly lower dipyridamole MBF compared to those with normal function.
Conclusions:
- Systolic dysfunction in HCM may be attributed to more severe impairments in coronary vasodilator capacity.
- Altered coronary vasodilator reserve is a potential mechanism underlying systolic dysfunction in hypertrophic cardiomyopathy.
Background:
We tested the hypothesis that a reduced delivery of blood to the myocardium is involved in the development of systolic dysfunction of patients with hypertrophic cardiomyopathy (HCM).
Methods And Results:
Eighty-four patients with HCM (62 men, age 43 +/- 12 years) were studied. Left ventricular dimensions and function (fractional shortening) were evaluated by 2-dimensional echocardiography. Myocardial blood flow (MBF) was measured by N13 -ammonia or O15 -water and positron emission tomography at baseline and after dipyridamole; coronary vasodilator reserve (CVR) was calculated as dipyridamole/baseline MBF. Patients with HCM in advanced New York Heart Association (NYHA) classes had lower dipyridamole MBF (NYHA class I = 1.57 +/- 0.64 vs class II = 1.52 +/- 0.58 vs class III = 0.96 +/- 0.32 mL/min per gram; analysis of variance, P <.05) and CVR (NYHA class I = 1.93 +/- 0.64 vs class II = 1.69 +/- 0.54 vs class III = 1.40 +/- 0.43; analysis of variance, P <.05). A positive linear correlation between fractional shortening and dipyridamole MBF was demonstrated (R = 0.23, P <.05), and patients with abnormal fractional shortening had lower dipyridamole MBF (1.07 +/- 0.43 vs 1.58 +/- 0.62 mL/min per gram, P <.01).
Conclusions:
Systolic dysfunction in HCM may be caused by a more severe alteration of the coronary vasodilator capacity.