Long-term follow-up of the primary hyperkinetic heart syndrome. An echocardiographic and hemodynamic study

Cesare Fiorentini, Maria T. Olivari, Paolo Moruzzi, Maurizio D. Guazzi

Research output: Contribution to journalArticle

Abstract

Anxiety, cardiac overactivity and hypercontractility, favorable response to beta-blockade characterize the primary hyperkinetic heart syndrome. Its natural history is unknown; evolution toward obstructive cardiomyopathy has been postulated. We undertook this study to evaluate the following: (1) the existence of a mutual potential between anxiety and cardiac overactivity and its contribution to the perpetuation of the disorder; (2) the development of hypertrophic subaortic stenosis and whether it represents a complication of the syndrome; and (3) the very prolonged normalization of the circulatory regimen by beta-blockade and whether it promotes an irreversible circulatory adjustment. Fourteen hyperkinetic patients were investigated by intravascular and ultrasound methods at their first admission and at yearly intervals in the subsequent five years. During this period seven of them were maintained untreated (group I) and seven received propranolol (group II). Interventricular septal and left ventricular posterior wall thickness (ultrasounds) and the ratio between the two were within normal limits in the control state and remained so for the duration of the follow-up, both in the treated (persistent circulatory normalization was documented) and in the untreated patients (cardiac hyperkinesis was unchanged or somewhat increased). Substitution of placebo for the active propranolol in group II, at the end of the follow-up, caused a prompt recurrence of the overactivity of the heart. It is concluded that (1) transition toward hypertrophic cardiomyopathy probably is not a feature of the syndrome; (2) propranolol does not produce an irreversible circulatory adjustment; (3) it is unlikely that a reciprocal potentiation between anxiety and cardiac overactivity perpetuate the disorder; if it did, then prolonged circulatory normalization could be expected to extinguish the syndrome.

Original languageEnglish
Pages (from-to)221-227
Number of pages7
JournalAmerican Journal of Medicine
Volume71
Issue number2
DOIs
Publication statusPublished - 1981

Fingerprint

Neurocirculatory Asthenia
Propranolol
Social Adjustment
Anxiety
Hemodynamics
Hyperkinesis
Hypertrophic Cardiomyopathy
Natural History
Cardiomyopathies
Pathologic Constriction
Placebos
Recurrence

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Long-term follow-up of the primary hyperkinetic heart syndrome. An echocardiographic and hemodynamic study. / Fiorentini, Cesare; Olivari, Maria T.; Moruzzi, Paolo; Guazzi, Maurizio D.

In: American Journal of Medicine, Vol. 71, No. 2, 1981, p. 221-227.

Research output: Contribution to journalArticle

Fiorentini, Cesare ; Olivari, Maria T. ; Moruzzi, Paolo ; Guazzi, Maurizio D. / Long-term follow-up of the primary hyperkinetic heart syndrome. An echocardiographic and hemodynamic study. In: American Journal of Medicine. 1981 ; Vol. 71, No. 2. pp. 221-227.
@article{8ca5dd1ceddd4bcb8728b773f3115e1a,
title = "Long-term follow-up of the primary hyperkinetic heart syndrome. An echocardiographic and hemodynamic study",
abstract = "Anxiety, cardiac overactivity and hypercontractility, favorable response to beta-blockade characterize the primary hyperkinetic heart syndrome. Its natural history is unknown; evolution toward obstructive cardiomyopathy has been postulated. We undertook this study to evaluate the following: (1) the existence of a mutual potential between anxiety and cardiac overactivity and its contribution to the perpetuation of the disorder; (2) the development of hypertrophic subaortic stenosis and whether it represents a complication of the syndrome; and (3) the very prolonged normalization of the circulatory regimen by beta-blockade and whether it promotes an irreversible circulatory adjustment. Fourteen hyperkinetic patients were investigated by intravascular and ultrasound methods at their first admission and at yearly intervals in the subsequent five years. During this period seven of them were maintained untreated (group I) and seven received propranolol (group II). Interventricular septal and left ventricular posterior wall thickness (ultrasounds) and the ratio between the two were within normal limits in the control state and remained so for the duration of the follow-up, both in the treated (persistent circulatory normalization was documented) and in the untreated patients (cardiac hyperkinesis was unchanged or somewhat increased). Substitution of placebo for the active propranolol in group II, at the end of the follow-up, caused a prompt recurrence of the overactivity of the heart. It is concluded that (1) transition toward hypertrophic cardiomyopathy probably is not a feature of the syndrome; (2) propranolol does not produce an irreversible circulatory adjustment; (3) it is unlikely that a reciprocal potentiation between anxiety and cardiac overactivity perpetuate the disorder; if it did, then prolonged circulatory normalization could be expected to extinguish the syndrome.",
author = "Cesare Fiorentini and Olivari, {Maria T.} and Paolo Moruzzi and Guazzi, {Maurizio D.}",
year = "1981",
doi = "10.1016/0002-9343(81)90115-7",
language = "English",
volume = "71",
pages = "221--227",
journal = "American Journal of Medicine",
issn = "0002-9343",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Long-term follow-up of the primary hyperkinetic heart syndrome. An echocardiographic and hemodynamic study

AU - Fiorentini, Cesare

AU - Olivari, Maria T.

AU - Moruzzi, Paolo

AU - Guazzi, Maurizio D.

PY - 1981

Y1 - 1981

N2 - Anxiety, cardiac overactivity and hypercontractility, favorable response to beta-blockade characterize the primary hyperkinetic heart syndrome. Its natural history is unknown; evolution toward obstructive cardiomyopathy has been postulated. We undertook this study to evaluate the following: (1) the existence of a mutual potential between anxiety and cardiac overactivity and its contribution to the perpetuation of the disorder; (2) the development of hypertrophic subaortic stenosis and whether it represents a complication of the syndrome; and (3) the very prolonged normalization of the circulatory regimen by beta-blockade and whether it promotes an irreversible circulatory adjustment. Fourteen hyperkinetic patients were investigated by intravascular and ultrasound methods at their first admission and at yearly intervals in the subsequent five years. During this period seven of them were maintained untreated (group I) and seven received propranolol (group II). Interventricular septal and left ventricular posterior wall thickness (ultrasounds) and the ratio between the two were within normal limits in the control state and remained so for the duration of the follow-up, both in the treated (persistent circulatory normalization was documented) and in the untreated patients (cardiac hyperkinesis was unchanged or somewhat increased). Substitution of placebo for the active propranolol in group II, at the end of the follow-up, caused a prompt recurrence of the overactivity of the heart. It is concluded that (1) transition toward hypertrophic cardiomyopathy probably is not a feature of the syndrome; (2) propranolol does not produce an irreversible circulatory adjustment; (3) it is unlikely that a reciprocal potentiation between anxiety and cardiac overactivity perpetuate the disorder; if it did, then prolonged circulatory normalization could be expected to extinguish the syndrome.

AB - Anxiety, cardiac overactivity and hypercontractility, favorable response to beta-blockade characterize the primary hyperkinetic heart syndrome. Its natural history is unknown; evolution toward obstructive cardiomyopathy has been postulated. We undertook this study to evaluate the following: (1) the existence of a mutual potential between anxiety and cardiac overactivity and its contribution to the perpetuation of the disorder; (2) the development of hypertrophic subaortic stenosis and whether it represents a complication of the syndrome; and (3) the very prolonged normalization of the circulatory regimen by beta-blockade and whether it promotes an irreversible circulatory adjustment. Fourteen hyperkinetic patients were investigated by intravascular and ultrasound methods at their first admission and at yearly intervals in the subsequent five years. During this period seven of them were maintained untreated (group I) and seven received propranolol (group II). Interventricular septal and left ventricular posterior wall thickness (ultrasounds) and the ratio between the two were within normal limits in the control state and remained so for the duration of the follow-up, both in the treated (persistent circulatory normalization was documented) and in the untreated patients (cardiac hyperkinesis was unchanged or somewhat increased). Substitution of placebo for the active propranolol in group II, at the end of the follow-up, caused a prompt recurrence of the overactivity of the heart. It is concluded that (1) transition toward hypertrophic cardiomyopathy probably is not a feature of the syndrome; (2) propranolol does not produce an irreversible circulatory adjustment; (3) it is unlikely that a reciprocal potentiation between anxiety and cardiac overactivity perpetuate the disorder; if it did, then prolonged circulatory normalization could be expected to extinguish the syndrome.

UR - http://www.scopus.com/inward/record.url?scp=0019374628&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019374628&partnerID=8YFLogxK

U2 - 10.1016/0002-9343(81)90115-7

DO - 10.1016/0002-9343(81)90115-7

M3 - Article

C2 - 7196153

AN - SCOPUS:0019374628

VL - 71

SP - 221

EP - 227

JO - American Journal of Medicine

JF - American Journal of Medicine

SN - 0002-9343

IS - 2

ER -