Limited maximal vasodilator capacity of forearm resistance vessels in patients with hypertrophic cardiomyopathy

Heart Vessels. 1990;5(3):159-65. doi: 10.1007/BF02059911.

Abstract

It is not known whether hypertrophic cardiomyopathy (HCM) is accompanied by an abnormality in vascular smooth muscles. In this study, we examined the maximal vasodilator capacity of forearm resistance vessels by measuring minimal forearm vascular resistance (min. FVR) during peak reactive hyperemia after 10 min of arterial occlusion in patients with HCM (n = 15, 41 +/- 4 years old) and age-matched control subjects (n = 12, 42 +/- 3 years old). Forearm blood flow (FBF) was measured by a mercury-in-silastic strain gauge plethysmograph and FVR was calculated by dividing mean blood pressure by FBF. Resting FBF was lower (P less than 0.05) and resting FVR was higher (P less than 0.01) in patients with HCM than in control subjects. Min. FVR was significantly greater in patients with HCM than in control subjects (2.7 +/- 0.2 vs 1.5 +/- 0.2 units, P less than 0.005). We also examined vasoconstrictive responses to intra-arterially infused angiotensin II (20 and 40 ng/min); responses were greater in patients with HCM than in control subjects (P less than 0.05). These results indicate that forearm circulation is altered in patients with HCM. The result that the maximal vasodilator capacity of forearm resistance vessels is limited in patients with HCM as compared with that in age-matched control subjects suggests that there may be abnormalities in forearm resistance vessels in patients with HCM, which might involve increased wall thickness or intrinsic abnormalities in vascular smooth muscle.

MeSH terms

  • Adult
  • Angiotensin II
  • Cardiomyopathy, Hypertrophic / physiopathology*
  • Female
  • Forearm / blood supply*
  • Humans
  • Hyperemia / physiopathology
  • Male
  • Muscle, Smooth, Vascular / physiology
  • Plethysmography
  • Regional Blood Flow
  • Vascular Resistance / physiology
  • Vasodilation / physiology*

Substances

  • Angiotensin II