Intravenous nitroglycerin in acute myocardial infarction.

Flaherty, John T.; Reid, Philip R.; Kelly, D T; Taylor, D R; Weisfeldt, Myron L.; Pitt, Bertram

doi:10.1161/01.cir.51.1.132

Cited by 308 publications

(56 citation statements)

References 17 publications

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“…In these experimental studies, myocardial damage was reduced with agents aimed at decreasing myocardial oxygen consumption (5-9), at increasing coronary flow either directly by reperfusion (10,11) or indirectly by enhancing collateral flow (5,6,12), by enhancinig anaerobic metabolism (13), and by the administration of hyaluronidase (14) and hydrocortisone (15). The application ofthese principles to the therapy of patients with acute myocardial infarction using some of these interventions seems to confirm these experimenital conclusions (4,6,(16)(17)(18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 67%

Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

Maroko¹,

Carpenter²,

Chiariello³

et al. 1978

J. Clin. Invest.

248

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Section: Introductionmentioning

confidence: 67%

Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

Maroko¹,

Carpenter²,

Chiariello³

et al. 1978

J. Clin. Invest.

248

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“…GTN is an effective therapeutic agent in the treatment of a number of cardiovascular disorders including myocardial ischaemia, myocardial infarction and congestive heart failure (Mason et al, 1971;Flaherty et al, 1975;Flaherty, 1983;Packer, 1983). The principal mechanism is a direct relaxation of vascular smooth muscle and a number of investigators believed that the effect on the venous capacitance vessels was more pronounced than on the arterial resistance vessels, while others have reported less marked differences.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular profile of 5 novel nitrate‐esters: a comparative study with nitroglycerin in pigs with and without left ventricular dysfunction

Woerkens

Giessen

Verdouw

1991

British J Pharmacology

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1 Four cumulative 10 min intravenous infusions of 0.05, 0.2, 0.5 and 2.0mg min I were used to compare the cardiovascular profile of 5 novel nitrate-esters dissolved in Intralipid 10% to that of nitroglycerin (GTN) in conscious pigs. 2 Infusion of Intralipid 10% alone had no effect on any of the systemic haemodynamic parameters. GTN infusions decreased mean arterial blood pressure dose-dependently from 94 + 2 mmHg to 79 + 3 mmHg (P <0.05) and raised cardiac output from 2.74 + 0.091 min' to 3.40 + 0.18 1 min' (P < 0.05) due to an increase in heart rate (by up to 43 + 3%), as stroke volume decreased slightly. Systemic vascular resistance decreased (by 32 ± 3%) and left ventricular end-diastolic pressure fell from 5.2 + 0.4 mmHg to 2.2 + 0.5 mmHg (both P < 0.05). 3 The novel compounds CEDO 8811, CEDO 8834 and CEDO 8901 increased cardiac output only at the highest dose (7%, 8% and 9%, respectively). There was no change in mean arterial blood pressure as the increase in cardiac output was counterbalanced by arterial vasodilatation. All three compounds reduced left ventricular end-diastolic pressure slightly. 4 CEDO 8816 was a more potent arterial and venodilator than the aforementioned CEDO cbmpounds, as the decreases in systemic vascular resistance and left ventricular end-diastolic pressure were already significant at lower doses. The fall in stroke volume was fully compensated by the increase in heart rate and as a result cardiac output increased by 11 + 3% (P < 0.05) at the highest dose. 5 CEDO 8956 was the most potent vasodilator of the novel compounds and exhibited a cardiovascular profile similar to that of GTN. Left ventricular end-diastolic pressure decreased significantly during infusion of 0.2mgmin-'. Mean arterial blood pressure decreased by 11 + 2% (P < 0.05) in spite of an increase in cardiac output by up to 20 ± 2% (P < 0.05), due to a decrease (by 27 + 1%, P < 0.05) in systemic vascular resistance. The increases in heart rate (20 ± 5%, P < 0.05) and LVdP/dtmax (38 + 4%, P < 0.05) were, however, considerably less after CEDO 8956 than after GTN. 6 The potential of CEDO 8956 in the treatment of chronic left ventricular dysfunction was evaluated during administration to conscious pigs (21-23 kg), in which the left circumflex coronary artery was ligated 4 weeks earlier. In these animals, baseline values for cardiac output and LVdP/dtx were lower and those of systemic vascular resistance and left ventricular end-diastolic pressure were higher than in the first group of experiments.7 Both GTN and CEDO 8956 in doses of 0.05 to 2.0 mg inm increased cardiac output dosedependently (by up to 34% and 19%, respectively). The decrease in systemic vascular resistance was larger with GTN (35%) than with CEDO 8956 (17%), which resulted in a 13% decrease in mean arterial pressure during infusion of GTN, whereas there was no change in mean arterial pressure during infusion of CEDO 8956. Both compounds increased LVdP/dt,,,,X (by 48% and 30%, respectively) and lowered left ventricular end-diastolic pressure to normal levels...

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“…Possible mechanisms include an increase in collateral blood flow to borderline ischemic myocardium due to (1) 17 hr after symptom onset. Forty-eight hour infusion of nitroprusside begun less than 9 hr after symptom onset resulted in a significantly higher short-term mortality as compared with placebo (24% vs 13%, respectively).…”

Section: Discussionmentioning

confidence: 99%

A randomized prospective trial of intravenous nitroglycerin in patients with acute myocardial infarction.

et al. 1983

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A prospective randomized study of intravenous nitroglycerin (TNG) administered for 48 hr after acute infarction was undertaken to determine whether clinical improvement and/or evidence of preservation of ischemic myocardium could be demonstrated. One hundred four patients were randomly assigned to TNG (n = 56) and placebo groups (n = 48). TNG was infused at a rate sufficient to lower mean arterial pressure 10%, monitored noninvasively. When all TNG-and placebo-treated patients were compared, no significant differences in clinical or laboratory outcomes could be demonstrated. TNG-and placebo-treated patients were retrospectively subdivided into early and late treatment groups (treatment begun <10 hr vs 3 10 hr after onset of symptoms). Early TNG treatment was associated with a lower incidence of infarct complications within the first 10 days, defined by new congestive heart failure, infarct extension, or cardiac death (15% in early TNG compared with a mean of 39% in the other three subgroups; p = .003). Mortality at 3 months was lower in the group treated early with TNG (15%) compared with a mean of 25% in the other three subgroups (p = NS). No significant differences were found in peak creatine kinase (CK) blood levels, creatine kinase infarct size, or preservation of precordial R waves by serial electrocardiographic mapping. Among 49 patients with pretreatment and day 7 to 14 posttreatment left ventricular ejection fraction measurements, improvement of 3 10% occurred in 35% of TNG patients treated early compared with 6% of those treated late with TNG, 11% of those treated early with placebo, and 0% of those treated late with placebo (p = .004). Similarly, in 68 patients in whom paired thallium scintigrams were taken, a decrease of B75% in the computer-determined thallium defect score was seen in 48% of TNG patients treated early, compared with 14% of TNG patients treated late, 33% of placebo patients treated early and 0% of placebo patients treated late (p = .039). Patients demonstrating significant scintigraphic improvement were treated earlier, tended to have less severe initial scintigraphic abnormalities, inferior rather than anterior infarctions, a longer history of angina, and no prior history of heart failure. Thus intravenous TNG could not be shown to result in significant improvement in clinical or scintigraphic outcomes when the patient population was analyzed as a whole. After retrospective subgroup analysis, intravenous TNG could be shown to protect ischemic myocardium in the subset of patients with smallto-moderate sized myocardial infarctions when treatment was begun within 10 hr of the onset of symptoms. The results of this trial also suggest that future clinical trials designed to show a reduction in infarct size might limit patient entry to those admitted early after symptom onset and those with significant abnormalities in their admission scintigraphic studies. Larger-scale studies are needed to determine whether TNG therapy can significantly reduce mortality and to further define the...

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Intravenous nitroglycerin in acute myocardial infarction.

Cited by 308 publications

References 17 publications

Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

Cardiovascular profile of 5 novel nitrate‐esters: a comparative study with nitroglycerin in pigs with and without left ventricular dysfunction

A randomized prospective trial of intravenous nitroglycerin in patients with acute myocardial infarction.

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