What does this research mean for the field?

Inotropic agents exert two opposing effects on acutely ischemic myocardium by increasing aneurysmal bulging during isometric contraction while improving wall velocity during ventricular ejection, demonstrating that ischemic tissue retains responsiveness to pharmacologic stimuli. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To evaluate the specific functional responses of acutely ischemic myocardial dyskinesis to various positive and negative inotropic agents.

June 1, 1974CirculationOpen Access

Effect of Inotropic Agents on the Localized Dyskinesis of Acutely Ischemic Myocardium

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Population

Open-chest anesthetized dogs with acute myocardial ischemia produced by coronary ligation

Design

Preclinical

Authors

RKRichard E. KerberAmerican College of Cardiology FAFrançois M. AbboudGeneral Cardiology MMMelvin L. MarcusCardiac Imaging

Discussion

Member takes

Implication

May increase ischemic bulging risk despite ejection gains; leaves open net effects in acute ischemia pending human studies.

Key Points

To evaluate the specific functional responses of acutely ischemic myocardial dyskinesis to various positive and negative inotropic agents.
Studied open-chest anesthetized dogs with acute posterior myocardial ischemia induced by coronary ligation and confirmed histologically.
Measured localized wall motion and velocity using direct-reflection ultrasound before and after intravenous administration of graded doses of isoproterenol, norepinephrine, ouabain, glucagon, and propranolol.
Aneurysmal bulging during isometric contraction significantly increased (P < 0.01) with isoproterenol (from 5 ± 0 to 6 ± 0 mm) and ouabain (from 4 ± 0 to 5 ± 0 mm).
Mean posterior wall velocity during ventricular ejection increased with isoproterenol (12 ± 1 to 26 ± 2 mm/sec), glucagon (12 ± 2 to 22 ± 2 mm/sec), norepinephrine (12 ± 1 to 17 ± 1 mm/sec), and ouabain (8 ± 1 to 12 ± 2 mm/sec).
Inotropic agents enhanced global hemodynamics, elevating cardiac output (glucagon > isoproterenol > ouabain) and left ventricular dp/dt (isoproterenol > glucagon > norepinephrine).

Structured PICO

Population

Open-chest anesthetized dogs with acute myocardial ischemia produced by coronary ligation

Intervention

Intravenous administration of graded doses of inotropic agents (isoproterenol, norepinephrine, ouabain, glucagon, and propranolol)

Outcome

Segmental dyskinesis (aneurysmal bulging during isometric contraction and mean posterior wall velocity during ventricular ejection)surrogate

In acutely ischemic myocardium, inotropic agents increase aneurysmal bulging during isometric contraction but improve wall velocity during ventricular ejection.

Cite This Study

Kerber et al. (1974) studied this question.

synapsesocial.com/papers/6a16ac65798df06fa4b268e3 https://doi.org/10.1161/01.cir.49.6.1038

Topics

Echocardiography

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June 1, 1974CirculationOpen Access

Effect of Inotropic Agents on the Localized Dyskinesis of Acutely Ischemic Myocardium

View Full Paper

Ask AI

Bookmark

Population

Open-chest anesthetized dogs with acute myocardial ischemia produced by coronary ligation

Design

Preclinical

Authors

RKRichard E. KerberAmerican College of Cardiology FAFrançois M. AbboudGeneral Cardiology MMMelvin L. MarcusCardiac Imaging

Discussion

Member takes

Implication

May increase ischemic bulging risk despite ejection gains; leaves open net effects in acute ischemia pending human studies.

Key Points

To evaluate the specific functional responses of acutely ischemic myocardial dyskinesis to various positive and negative inotropic agents.
Studied open-chest anesthetized dogs with acute posterior myocardial ischemia induced by coronary ligation and confirmed histologically.
Measured localized wall motion and velocity using direct-reflection ultrasound before and after intravenous administration of graded doses of isoproterenol, norepinephrine, ouabain, glucagon, and propranolol.
Aneurysmal bulging during isometric contraction significantly increased (P < 0.01) with isoproterenol (from 5 ± 0 to 6 ± 0 mm) and ouabain (from 4 ± 0 to 5 ± 0 mm).
Mean posterior wall velocity during ventricular ejection increased with isoproterenol (12 ± 1 to 26 ± 2 mm/sec), glucagon (12 ± 2 to 22 ± 2 mm/sec), norepinephrine (12 ± 1 to 17 ± 1 mm/sec), and ouabain (8 ± 1 to 12 ± 2 mm/sec).
Inotropic agents enhanced global hemodynamics, elevating cardiac output (glucagon > isoproterenol > ouabain) and left ventricular dp/dt (isoproterenol > glucagon > norepinephrine).

Structured PICO

Population

Open-chest anesthetized dogs with acute myocardial ischemia produced by coronary ligation

Intervention

Intravenous administration of graded doses of inotropic agents (isoproterenol, norepinephrine, ouabain, glucagon, and propranolol)

Outcome

Segmental dyskinesis (aneurysmal bulging during isometric contraction and mean posterior wall velocity during ventricular ejection)surrogate

In acutely ischemic myocardium, inotropic agents increase aneurysmal bulging during isometric contraction but improve wall velocity during ventricular ejection.

Cite This Study

Kerber et al. (1974) studied this question.

synapsesocial.com/papers/6a16ac65798df06fa4b268e3 https://doi.org/10.1161/01.cir.49.6.1038

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

Topics

Echocardiography

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