Transdermal Nitroglycerin Patch Therapy Improves Left Ventricular Function and Prevents Remodeling After Acute Myocardial Infarction

Mahmarian, John J.; Moyé, Lemuel A.; Chinoy, David A.; Sequeira, Rafael F.; Habib, Gabriel B.; Henry, Walter J.; Jain, Avanindra; Chaitman, Bernard R.; Weng, Cui-Lian; Morales-Ballejo, Hugo; Pratt, Craig M.

doi:10.1161/01.cir.97.20.2017

Cited by 48 publications

(16 citation statements)

References 36 publications

(34 reference statements)

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“…58,59,85 Transient ST changes (≥0.5 mm [0.05 mV]) during symptoms at rest strongly suggest ischemia and underlying severe CAD. Patients without acute ischemic changes on ECG have a reduced risk of MI and a very low risk of inhospital life-threatening complications, even in the presence of confounding electrocardiographic patterns such as LV hypertrophy.…”

Section: Electrocardiogrammentioning

confidence: 99%

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

Amsterdam¹,

Wenger²,

Brindis³

et al. 2014

Circulation

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904

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Section: Electrocardiogrammentioning

confidence: 99%

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

Amsterdam¹,

Wenger²,

Brindis³

et al. 2014

Circulation

1,056

904

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“…40 The long-term beneficial effects of transdermal nitroglycerin on left ventricular remodeling after myocardial infarction have also been reported. 41 Despite these positive results, the large GISSI-3 trial (Gruppo Italiano per lo Studio della Sopravvivenza nell'infarto Miocardico) 42 and the Fourth International Study of Infarct Survival (ISIS 4) 43 failed to show a significant mortality benefit in patients treated with nitrates after acute myocardial infarction. This may have been due to a null bias related to extensive use of nonstudy nitrates and also to the limited efficacy of the nitrate regimens used.…”

Section: Nitroglycerinmentioning

confidence: 99%

Left Ventricular Remodeling After Myocardial Infarction

2000

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L eft ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. 1,2 Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease ( Figure 1). This article will review postinfarction remodeling, pathophysiological mechanisms, and therapeutic intervention. Pathophysiology Postinfarction Left Ventricular RemodelingThe acute loss of myocardium results in an abrupt increase in loading conditions that induces a unique pattern of remodeling involving the infarcted border zone and remote noninfarcted myocardium. Myocyte necrosis and the resultant increase in load trigger a cascade of biochemical intracellular signaling processes that initiates and subsequently modulates reparative changes, which include dilatation, hypertrophy, and the formation of a discrete collagen scar. Ventricular remodeling may continue for weeks or months until the distending forces are counterbalanced by the tensile strength of the collagen scar. This balance is determined by the size, location, and transmurality of the infarct, the extent of myocardial stunning, the patency of the infarct-related artery, and local tropic factors. 1,3 The myocardium consists of 3 integrated components: myocytes, extracellular matrix, and the capillary microcirculation that services the contractile unit assembly. Consideration of all 3 components provides important insights into the remodeling process and a rationale for future therapeutic strategies. The cardiomyocyte is terminally differentiated and develops tension by shortening. The extracellular matrix provides a stress-tolerant, viscoelastic scaffold consisting of type I and type III collagen that couples myocytes and maintains the spatial relations between the myofilaments and their capillary microcirculation. 4,5 The collagen framework couples adjacent myocytes by intercellular struts that align myofilaments to optimize force development, distribute force evenly to the ventricular walls, and prevent sarcomeric deformation. 5 Myocardial infarction results in the migration of macrophages, monocytes, and neutrophils into the infarct zone; this initiates intracellular signaling and neurohormonal activation, which localizes the inflammatory response. Changes in circulatory hemodynamics are determined primarily by the magnitude of myocyte loss, the stimulation of the sympathetic nervous system and renin-angiotensin-aldosterone system, and the release of natriuretic peptides.Postinfarction remodeling has been arbitrarily divided into an early phase (within 72 hours) and a late phase (beyond 72 hours). The early phase involves expansion of the infarct zone, 5 which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. The failure to normalize increa...

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“…Beta-blockers (BB) (1), angiotensin-converting enzyme (ACE) inhibitors (2), antiplatelet agents (3), statins (4), and certain rate-lowering calcium-channel blockers (CCB) (5) benefit patients through their targeted effects on thrombus formation (6,7), plaque progression (8), myocardial ischemia (9), and left ventricular (LV) dysfunction and remodeling (10). However, despite this extensive trial-based evidence, coronary revascularization is generally considered the preferred treatment for patients after AMI, particularly when there is extensive coronary artery disease (CAD) on angiography or substantial myocardial ischemia detected by noninvasive testing.…”

mentioning

confidence: 99%

An Initial Strategy of Intensive Medical Therapy Is Comparable to That of Coronary Revascularization for Suppression of Scintigraphic Ischemia in High-Risk But Stable Survivors of Acute Myocardial Infarction

Mahmarian

Dakik

Filipchuk

et al. 2006

Journal of the American College of Cardiology

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Transdermal Nitroglycerin Patch Therapy Improves Left Ventricular Function and Prevents Remodeling After Acute Myocardial Infarction

Cited by 48 publications

References 36 publications

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes

Left Ventricular Remodeling After Myocardial Infarction

An Initial Strategy of Intensive Medical Therapy Is Comparable to That of Coronary Revascularization for Suppression of Scintigraphic Ischemia in High-Risk But Stable Survivors of Acute Myocardial Infarction

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