Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location.

Jugdutt, Bodh I.; Warnica, J. Wayne

doi:10.1161/01.cir.78.4.906

Cited by 364 publications

(133 citation statements)

References 26 publications

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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.…”

Section: Nitroglycerinmentioning

confidence: 97%

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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Section: Nitroglycerinmentioning

confidence: 97%

Left Ventricular Remodeling After Myocardial Infarction

2000

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“…In addition five trials of oral nitrates have been published (Fitzgerald & Bennet, 1990;Mellen et al, 1967;Newell & clinical collaborators, 1970;Oscharoff, 1964;Ryan & Schnee, 1965 (Jugdutt & Warnica, 1988). The other trial followed 60 patients for 18 months and reported a 4/31 (13%) mortality in actively treated patients and 12/29 (41%) in control patients (P <0.02) (Bussmann etal., 1981 (Yusuf et al, 1988).…”

Section: Acute Myocardial Infarctionmentioning

confidence: 99%

“…Myocardial infarct size, estimated from creatine kinase (CK) enzyme profiles, was significantly reduced by about one third in patients with nitrates compared with controls in three of the intravenous trials that provided such data (Bussmann et al, 1981;Jaffe et al, 1983;Jugdutt & Warnica, 1988). One other trial compared peak CK enzyme levels of treated and control patients but did not find any difference between the groups (Flaherty et al, 1983).…”

Section: Acute Myocardial Infarctionmentioning

confidence: 99%

Effects of nitrates on mortality in acute myocardial infarction and in heart failure.

Held¹

1992

Brit J Clinical Pharma

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“…[2][3][4][5] Consequently, nitrates are widely used for the treatment of MI in forms ranging from sublingual to transdermal and intravenous. [6][7][8] Two large multicenter studies, Gruppo Italiano per lo Studio della Sopravvivenza nell' Infarto Miocardico (GISSI-3) and the Fourth International Study of Infarct Survival (ISIS-4), dealt with the effects of nitrates on mortality following MI. 9,10 These two megatrials, in fact, demonstrated no significant decrease in mortality in the nitrate-treated group; merely a small decrease was noted in 6-week mortality, which did not reach a level of significance (for 1,000 patients, this decrease was 2.1 in ISIS-4, and 3.9 in GISSI-3).…”

Section: Introductionmentioning

confidence: 99%

Effects of long‐term transdermal nitrate treatment on left ventricular function in patients following myocardial infarction

Király

Kiss

Timár

et al. 2003

Clinical Cardiology

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SummaryBackground: Nitrates are widely used for the treatment of myocardial infarction (MI). The large megatrials (GISSI-3 and ISIS-4) did not in fact demonstrate a significant decrease in mortality in the nitrate-treated group. However, examination of the number of postinfarction angina episodes and the occurrence of cardiogenic shock in the GISSI-3 study did reveal significant decreases.Hypothesis: It was hypothesized that chronic nitrate treatment after an MI preserves left ventricular systolic and/or diastolic functions.Methods: Patients were divided into two groups: those receiving chronic nitrate treatment for 6 months after an MI (n = 30), and those without such treatment (n = 29). Echocardiography was performed 3, 14, 42, and 180 days after the infarction. The changes in early diastolic and atrial contractionrelated mitral valve inflow pattern and deceleration time were assayed. Alterations in systolic, diastolic, and atrial reverse flow velocities in the pulmonary vein were measured, as were ejection fraction (EF), the number of registered angina episodes, and the maximal ST-segment depression in response to the stress test.Results: During the 6-month study period, the increase in systolic pulmonary venous flow velocity was significantly larger in the nitrate group than in the controls. The decreases in the velocities of the diastolic and the atrial reverse flow were also more pronounced in the nitrate group than in the controls.

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Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location.

Abstract: To determine 1) whether the effect of intravenous nitroglycerin (NG) therapy during acute myocardial infarction on creatine kinase infarct size is influenced by infarct location (anterior vs.

Cited by 364 publications

References 26 publications

Left Ventricular Remodeling After Myocardial Infarction

Left Ventricular Remodeling After Myocardial Infarction

Effects of nitrates on mortality in acute myocardial infarction and in heart failure.

Effects of long‐term transdermal nitrate treatment on left ventricular function in patients following myocardial infarction

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