Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function

R. Lorenzoni, R. Gistri, F. Cecchi, I. Olivotto, G. Chiriatti, P. Elliott, W. J. McKenna, P. G. Camici

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Non-sustained ventricular tachycardia on Holter and syncope have been considered risk factors for sudden death in hypertrophic cardiomyopathy. Aims. In these patients the coronary vasodilator reserve is impaired despite normal coronaries, so we evaluated the correlation between the severity of coronary vasodilator reserve impairment and the occurrence of syncope and non-sustained ventricular tachycardia. Methods and Results. Eighty-four patients with hypertrophic cardiomyopathy (62 males, age 43 ± 12 years) had a two-dimensional echocardiographic study and a 48-h Holter. Myocardial blood flow was measured by positron emission tomography, at baseline and after dipyridamole, and the coronary vasodilator reserve was computed as dipyridamole myocardial blood flow/baseline myocardial blood flow. In 27 patients, subendocardial and subepicardial myocardial blood flow was measured in the septum and the subendocardial/subepicardial ratio was computed. Twenty of 84 patients had at least one syncopal episode, and 26 had at least one run of non-sustained ventricular tachycardia on Holter. Baseline and dipyridamole myocardial blood flow, coronary vasodilator reserve, and baseline and dipyridamole subendocardial/subepicardial myocardial blood flow ratio were similar in patients with and without syncope and with and without non-sustained ventricular tachycardia on Holter. However, patients with non-sustained ventricular tachycardia had larger left ventricular end-diastolic (47 ± 6 vs 44 ± 5 mm, P <0.05) and end-systolic diameters (30 ± 6 vs 27 ± 3 mm, P <0.05). Conclusions. (1) Coronary vasodilation is not more severely impaired in patients with hypertrophic cardiomyopathy and syncope or non-sustained ventricular tachycardia. (2) The left ventricle is more dilated in hypertrophic cardiomyopathy with non-sustained ventricular tachycardia.

Original languageEnglish
Pages (from-to)1946-1950
Number of pages5
JournalEuropean Heart Journal
Volume18
Issue number12
Publication statusPublished - 1997

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Hypertrophic Cardiomyopathy
Syncope
Ventricular Tachycardia
Cardiac Arrhythmias
Dipyridamole
Vasodilator Agents
Sudden Death
Vasodilation
Positron-Emission Tomography
Heart Ventricles

Keywords

  • Hypertrophic cardiomyopathy
  • Myocardial blood flow
  • Positron emission tomography
  • Ventricular tachycardia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function. / Lorenzoni, R.; Gistri, R.; Cecchi, F.; Olivotto, I.; Chiriatti, G.; Elliott, P.; McKenna, W. J.; Camici, P. G.

In: European Heart Journal, Vol. 18, No. 12, 1997, p. 1946-1950.

Research output: Contribution to journalArticle

Lorenzoni, R, Gistri, R, Cecchi, F, Olivotto, I, Chiriatti, G, Elliott, P, McKenna, WJ & Camici, PG 1997, 'Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function', European Heart Journal, vol. 18, no. 12, pp. 1946-1950.
Lorenzoni, R. ; Gistri, R. ; Cecchi, F. ; Olivotto, I. ; Chiriatti, G. ; Elliott, P. ; McKenna, W. J. ; Camici, P. G. / Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function. In: European Heart Journal. 1997 ; Vol. 18, No. 12. pp. 1946-1950.
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T1 - Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function

AU - Lorenzoni, R.

AU - Gistri, R.

AU - Cecchi, F.

AU - Olivotto, I.

AU - Chiriatti, G.

AU - Elliott, P.

AU - McKenna, W. J.

AU - Camici, P. G.

PY - 1997

Y1 - 1997

N2 - Non-sustained ventricular tachycardia on Holter and syncope have been considered risk factors for sudden death in hypertrophic cardiomyopathy. Aims. In these patients the coronary vasodilator reserve is impaired despite normal coronaries, so we evaluated the correlation between the severity of coronary vasodilator reserve impairment and the occurrence of syncope and non-sustained ventricular tachycardia. Methods and Results. Eighty-four patients with hypertrophic cardiomyopathy (62 males, age 43 ± 12 years) had a two-dimensional echocardiographic study and a 48-h Holter. Myocardial blood flow was measured by positron emission tomography, at baseline and after dipyridamole, and the coronary vasodilator reserve was computed as dipyridamole myocardial blood flow/baseline myocardial blood flow. In 27 patients, subendocardial and subepicardial myocardial blood flow was measured in the septum and the subendocardial/subepicardial ratio was computed. Twenty of 84 patients had at least one syncopal episode, and 26 had at least one run of non-sustained ventricular tachycardia on Holter. Baseline and dipyridamole myocardial blood flow, coronary vasodilator reserve, and baseline and dipyridamole subendocardial/subepicardial myocardial blood flow ratio were similar in patients with and without syncope and with and without non-sustained ventricular tachycardia on Holter. However, patients with non-sustained ventricular tachycardia had larger left ventricular end-diastolic (47 ± 6 vs 44 ± 5 mm, P <0.05) and end-systolic diameters (30 ± 6 vs 27 ± 3 mm, P <0.05). Conclusions. (1) Coronary vasodilation is not more severely impaired in patients with hypertrophic cardiomyopathy and syncope or non-sustained ventricular tachycardia. (2) The left ventricle is more dilated in hypertrophic cardiomyopathy with non-sustained ventricular tachycardia.

AB - Non-sustained ventricular tachycardia on Holter and syncope have been considered risk factors for sudden death in hypertrophic cardiomyopathy. Aims. In these patients the coronary vasodilator reserve is impaired despite normal coronaries, so we evaluated the correlation between the severity of coronary vasodilator reserve impairment and the occurrence of syncope and non-sustained ventricular tachycardia. Methods and Results. Eighty-four patients with hypertrophic cardiomyopathy (62 males, age 43 ± 12 years) had a two-dimensional echocardiographic study and a 48-h Holter. Myocardial blood flow was measured by positron emission tomography, at baseline and after dipyridamole, and the coronary vasodilator reserve was computed as dipyridamole myocardial blood flow/baseline myocardial blood flow. In 27 patients, subendocardial and subepicardial myocardial blood flow was measured in the septum and the subendocardial/subepicardial ratio was computed. Twenty of 84 patients had at least one syncopal episode, and 26 had at least one run of non-sustained ventricular tachycardia on Holter. Baseline and dipyridamole myocardial blood flow, coronary vasodilator reserve, and baseline and dipyridamole subendocardial/subepicardial myocardial blood flow ratio were similar in patients with and without syncope and with and without non-sustained ventricular tachycardia on Holter. However, patients with non-sustained ventricular tachycardia had larger left ventricular end-diastolic (47 ± 6 vs 44 ± 5 mm, P <0.05) and end-systolic diameters (30 ± 6 vs 27 ± 3 mm, P <0.05). Conclusions. (1) Coronary vasodilation is not more severely impaired in patients with hypertrophic cardiomyopathy and syncope or non-sustained ventricular tachycardia. (2) The left ventricle is more dilated in hypertrophic cardiomyopathy with non-sustained ventricular tachycardia.

KW - Hypertrophic cardiomyopathy

KW - Myocardial blood flow

KW - Positron emission tomography

KW - Ventricular tachycardia

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