Hemodynamic, left ventricular structural and hormonal changes after discrete myocardial damage in the dog

Kenneth M. McDonald, Gary S. Francis, Peter F. Carlyle, Kate Hauer, John Matthews, David W. Hunter, Jay N. Cohn

Research output: Contribution to journalArticle

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Abstract

Transmyocardial direct-current (DC) shock produces localized left ventricular myocardial necrosis without obstruction to coronary blood flow. In 43 dogs sequential measurements of hemodynamic, neuroendocrine and myocardial structural changes were made at baseline and for 16 weeks after DC shock. Six dogs (14%) died in the peri-shock period. By 1 week after shock, left ventricular mass, as measured by nuclear magnetic resonance imaging, had increased from a mean value ± SD of 67.9 ± 10.1 to 82.5 ± 12.9 g (p = 0.0001). Left ventricular end-diastolic volume was unchanged at 1 week but increased at 16 weeks from 56.1 ± 10.3 to 70.3 ± 10.7 ml (p = 0.0003). Left ventricular mass demonstrated a further increase at 12 months (107.8 ± 14.8 g). Rest cardiac output was significantly decreased at 4 months (3.67 ± 1.23 to 3.18 ± 0.81 liters/min, p < 0.01) as was stroke volume (43 ± 9 to 37 ± 7 ml, p ≤ 0.01). Left ventricular ejection fraction decreased progressively from 73% to 38% at 1 year. At 4 months there were increases in mean pulmonary artery pressure (18 ± 4 to 23 ± 4 mm Hg, p < 0.01), pulmonary capillary wedge pressure (9 ± 3 to 15 ± 3 mm Kg, p < 0.01) and right atrial pressure (5 ± 4 to 9 ± 3 mm Hg, p < 0.01). Plasma norepinephrine was increased at 4 months (318 ± 190 to 523 ± 221 pg/ml, p = 0.0003), whereas plasma renin activity was not significantly changed (4.3 ± 2.6 vs. 5.2 ± 3.4 ng/ml per h). Microsphere regional blood flow studies demonstrated a 50% reduction in skeletal muscle blood flow at 4 months (0.06 ± 0.06 ml/min per g compared with 0.12 ± 0.09 in normal dogs, p = 0.05), and a reduction in the endocardial/epicardial blood flow ratio (1.11 ± 0.13 compared with 1.24 ± 0.13 in normal dogs, p = 0.02). Therefore, in this model of acute left ventricular damage, left ventricular hypertrophy precedes progressive left ventricular dilation. The hemodynamic and hormonal changes mimic the pattern observed in patients who develop left ventricular dysfunction after myocardial infarction and the model thus provides a unique opportunity to study physiologic and pharmacologic responses during this period.

Original languageEnglish (US)
Pages (from-to)460-467
Number of pages8
JournalJournal of the American College of Cardiology
Volume19
Issue number2
DOIs
StatePublished - Jan 1 1992

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Shock
Hemodynamics
Dogs
Stroke Volume
Pulmonary Wedge Pressure
Atrial Pressure
Regional Blood Flow
Left Ventricular Dysfunction
Left Ventricular Hypertrophy
Microspheres
Renin
Cardiac Output
Pulmonary Artery
Dilatation
Norepinephrine
Skeletal Muscle
Necrosis
Magnetic Resonance Spectroscopy
Myocardial Infarction
Magnetic Resonance Imaging

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Hemodynamic, left ventricular structural and hormonal changes after discrete myocardial damage in the dog. / McDonald, Kenneth M.; Francis, Gary S.; Carlyle, Peter F.; Hauer, Kate; Matthews, John; Hunter, David W.; Cohn, Jay N.

In: Journal of the American College of Cardiology, Vol. 19, No. 2, 01.01.1992, p. 460-467.

Research output: Contribution to journalArticle

McDonald, Kenneth M. ; Francis, Gary S. ; Carlyle, Peter F. ; Hauer, Kate ; Matthews, John ; Hunter, David W. ; Cohn, Jay N. / Hemodynamic, left ventricular structural and hormonal changes after discrete myocardial damage in the dog. In: Journal of the American College of Cardiology. 1992 ; Vol. 19, No. 2. pp. 460-467.
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N2 - Transmyocardial direct-current (DC) shock produces localized left ventricular myocardial necrosis without obstruction to coronary blood flow. In 43 dogs sequential measurements of hemodynamic, neuroendocrine and myocardial structural changes were made at baseline and for 16 weeks after DC shock. Six dogs (14%) died in the peri-shock period. By 1 week after shock, left ventricular mass, as measured by nuclear magnetic resonance imaging, had increased from a mean value ± SD of 67.9 ± 10.1 to 82.5 ± 12.9 g (p = 0.0001). Left ventricular end-diastolic volume was unchanged at 1 week but increased at 16 weeks from 56.1 ± 10.3 to 70.3 ± 10.7 ml (p = 0.0003). Left ventricular mass demonstrated a further increase at 12 months (107.8 ± 14.8 g). Rest cardiac output was significantly decreased at 4 months (3.67 ± 1.23 to 3.18 ± 0.81 liters/min, p < 0.01) as was stroke volume (43 ± 9 to 37 ± 7 ml, p ≤ 0.01). Left ventricular ejection fraction decreased progressively from 73% to 38% at 1 year. At 4 months there were increases in mean pulmonary artery pressure (18 ± 4 to 23 ± 4 mm Hg, p < 0.01), pulmonary capillary wedge pressure (9 ± 3 to 15 ± 3 mm Kg, p < 0.01) and right atrial pressure (5 ± 4 to 9 ± 3 mm Hg, p < 0.01). Plasma norepinephrine was increased at 4 months (318 ± 190 to 523 ± 221 pg/ml, p = 0.0003), whereas plasma renin activity was not significantly changed (4.3 ± 2.6 vs. 5.2 ± 3.4 ng/ml per h). Microsphere regional blood flow studies demonstrated a 50% reduction in skeletal muscle blood flow at 4 months (0.06 ± 0.06 ml/min per g compared with 0.12 ± 0.09 in normal dogs, p = 0.05), and a reduction in the endocardial/epicardial blood flow ratio (1.11 ± 0.13 compared with 1.24 ± 0.13 in normal dogs, p = 0.02). Therefore, in this model of acute left ventricular damage, left ventricular hypertrophy precedes progressive left ventricular dilation. The hemodynamic and hormonal changes mimic the pattern observed in patients who develop left ventricular dysfunction after myocardial infarction and the model thus provides a unique opportunity to study physiologic and pharmacologic responses during this period.

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