Effects of nitroglycerin on left ventricular cavitary size and cardiac performance determined by ultrasound in man

Anthony N. DeMaria, Louis A. Vismara, Karen Auditore, Ezra A Amsterdam, Robert Zelis, Dean T. Mason

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

Controversy remains whether the antianginal action of nitroglycerin is the result of change in coronary blood flow or decrease in myocardial oxygen demand (MVO2) by decline in left ventricular systolic tension. Although left ventricular radius is an important determinant of left ventricular tension, clinical data have not been available on the effects of nitroglycerin on left ventricular cavitary size. Thus we evaluated the action of the organic nitrate on endocardial left ventricular dimensions determined by echograms. Left ventricular echoes were obtained just below the mitral valve in 6 normal subjects and in 14 patients with coronary disease before and at 2 minute intervals for 10 minutes after the sublingual administration of 0.6 mg nitroglycerin. Mean heart rate rose from 71 to 83 beats/min (p < 0.001) and mean arterial pressure fell from 92 to 87 mm Hg (p < 0.001) whereas cardiac output and peripheral vascular resistance were not significantly altered. Nitroglycerin reduced left ventricular end-diastolic dimension (4.94 to 4.69 cm, p < 0.001) and end-systolic dimension (3.63 to 3.37 cm, p < 0.001) accounting for declines in calculated left ventricular end-diastolic volume (129 to 112 cc, p < 0.001) and end-systolic volume (57 to 47 cc, p < 0.001) with fall in stroke volume from 72 to 65 cc, p < 0.01. Mean fiber shortening velocity (VCF) decreased from 1.08 to 1.02 circumferences/sec (p < 0.01), indicating reduced preload as we found with VCF on head-up tilting. Since stroke volume fell in patients with minimal changes in heart rate whereas peripheral vascular resistance remained unaltered, the principal extracardiac dilator effect of nitroglycerin is on the systemic venous bed. Thus, sublingual administration of nitroglycerin in man reduces end-diastolic dimension and end-systolic dimension and thereby is capable of lowering MVO2 by diminishing left ventricular tension. These findings support the concept that a decrease in MVO2 plays an important role in the relief of angina pectoris by nitroglycerin.

Original languageEnglish (US)
Pages (from-to)754-760
Number of pages7
JournalThe American journal of medicine
Volume57
Issue number5
DOIs
StatePublished - 1974

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Nitroglycerin
Vascular Resistance
Sublingual Administration
Stroke Volume
Heart Rate
Angina Pectoris
Mitral Valve
Cardiac Output
Nitrates
Coronary Disease
Arterial Pressure
Head
Oxygen

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Effects of nitroglycerin on left ventricular cavitary size and cardiac performance determined by ultrasound in man. / DeMaria, Anthony N.; Vismara, Louis A.; Auditore, Karen; Amsterdam, Ezra A; Zelis, Robert; Mason, Dean T.

In: The American journal of medicine, Vol. 57, No. 5, 1974, p. 754-760.

Research output: Contribution to journalArticle

DeMaria, Anthony N. ; Vismara, Louis A. ; Auditore, Karen ; Amsterdam, Ezra A ; Zelis, Robert ; Mason, Dean T. / Effects of nitroglycerin on left ventricular cavitary size and cardiac performance determined by ultrasound in man. In: The American journal of medicine. 1974 ; Vol. 57, No. 5. pp. 754-760.
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AB - Controversy remains whether the antianginal action of nitroglycerin is the result of change in coronary blood flow or decrease in myocardial oxygen demand (MVO2) by decline in left ventricular systolic tension. Although left ventricular radius is an important determinant of left ventricular tension, clinical data have not been available on the effects of nitroglycerin on left ventricular cavitary size. Thus we evaluated the action of the organic nitrate on endocardial left ventricular dimensions determined by echograms. Left ventricular echoes were obtained just below the mitral valve in 6 normal subjects and in 14 patients with coronary disease before and at 2 minute intervals for 10 minutes after the sublingual administration of 0.6 mg nitroglycerin. Mean heart rate rose from 71 to 83 beats/min (p < 0.001) and mean arterial pressure fell from 92 to 87 mm Hg (p < 0.001) whereas cardiac output and peripheral vascular resistance were not significantly altered. Nitroglycerin reduced left ventricular end-diastolic dimension (4.94 to 4.69 cm, p < 0.001) and end-systolic dimension (3.63 to 3.37 cm, p < 0.001) accounting for declines in calculated left ventricular end-diastolic volume (129 to 112 cc, p < 0.001) and end-systolic volume (57 to 47 cc, p < 0.001) with fall in stroke volume from 72 to 65 cc, p < 0.01. Mean fiber shortening velocity (VCF) decreased from 1.08 to 1.02 circumferences/sec (p < 0.01), indicating reduced preload as we found with VCF on head-up tilting. Since stroke volume fell in patients with minimal changes in heart rate whereas peripheral vascular resistance remained unaltered, the principal extracardiac dilator effect of nitroglycerin is on the systemic venous bed. Thus, sublingual administration of nitroglycerin in man reduces end-diastolic dimension and end-systolic dimension and thereby is capable of lowering MVO2 by diminishing left ventricular tension. These findings support the concept that a decrease in MVO2 plays an important role in the relief of angina pectoris by nitroglycerin.

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