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Hemodynamic changes and prognosis in patients with hypertrophic cardiomyopathy and abnormal blood pressure responses

Mitsuru Nagata1, Masami Shimizu, Hidekazu Ino

  • 1Molecular Genetics of Cardiovascular Disorders, Division of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.

Clinical Cardiology
|March 11, 2003
PubMed

Insights

Abnormal blood pressure response (BPR) during exercise in hypertrophic cardiomyopathy (HCM) patients is linked to a higher risk of cardiac events. This may be due to a lack of stroke volume increase, not heart rate or vascular resistance changes.

Area of Science:

  • Cardiology
  • Exercise Physiology
  • Clinical Medicine

Background:

  • Abnormal blood pressure response (BPR) during exercise is a potential risk factor for sudden cardiac death in hypertrophic cardiomyopathy (HCM) patients.
  • Some HCM patients exhibit systolic dysfunction during exercise, highlighting the need for further investigation into exercise hemodynamics.

Purpose of the Study:

  • To investigate the hemodynamic response during exercise in patients with HCM and abnormal BPR.
  • To clarify the long-term prognosis for HCM patients experiencing abnormal BPR during exercise.

Main Methods:

  • Sixty-five HCM patients underwent radionuclide monitoring of left ventricular function and blood pressure measurements during supine ergometer exercise.
  • Cardiac events were prospectively recorded for an average follow-up period of 76 months.

Main Results:

  • Seven out of 65 patients (11%) exhibited abnormal BPR; the remaining had normal BPR.
  • Stroke volume failed to increase in the abnormal BPR group, unlike the normal BPR group.
  • Patients with abnormal BPR had a significantly higher incidence of malignant arrhythmias (43%) compared to those with normal BPR (2%) during follow-up.

Conclusions:

  • Abnormal BPR in nonobstructive HCM is associated with a high prevalence of cardiac events.
  • The primary predictor of abnormal BPR during exercise appears to be an inadequate increase in stroke volume, rather than alterations in systemic vascular resistance or heart rate.
Abstract

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