ST elevation myocardial infarction nitrate therapy
| Myocardial infarction | |
| ICD-10 | I21-I22 |
|---|---|
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
| Cardiology Network |
 Discuss ST elevation myocardial infarction nitrate therapy further in the WikiDoc Cardiology Network |
| Adult Congenital |
|---|
| Biomarkers |
| Cardiac Rehabilitation |
| Congestive Heart Failure |
| CT Angiography |
| Echocardiography |
| Electrophysiology |
| Cardiology General |
| Genetics |
| Health Economics |
| Hypertension |
| Interventional Cardiology |
| MRI |
| Nuclear Cardiology |
| Peripheral Arterial Disease |
| Prevention |
| Public Policy |
| Pulmonary Embolism |
| Stable Angina |
| Valvular Heart Disease |
| Vascular Medicine |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Nitroglycerin
Mechanism(s) of Benefit
In determining whether nitrates should be administered and in determining the dose, the following mechanisms of benefit (as well as potential for harm) associated with nitrate administration should be kept in mind:
- 1. Reduction in preload via venodilation. While this may be of benefit in many STEMI patients, this may lead to hypotension and hypoperfusion in those patients with right ventricular infarction with ST segment elevation in lead V4R.
- 2. Reduction in afterload via arterial dilation. This may be of particular relevance in the patient with pulmonary edema or papillary muscle rupture or other mechanical complications.
- 3. Vasodilation of epicardial coronary arteries. While a modest component of vasoconstriction may be present in the majority of STEMI patients, relief of vasospasm may be particularly important in those rare patients with coronary spasm as the precipitating event.
- 4. Dilation of collateral vessels. This vasodilatory benefit must, however, be balanced against the load dependence of collateral filling and optimization of the subendocardial to epicardial flow ratio [1] [2] [3]
Clinical Trial Data
A large, definitive, randomized trial of nitrate administration (ISIS 4) demonstrated no significant mortality benefit of acute nitrate administration. Similarly, a pooled analysis involving more than 80.000 patients treated with nitrates either intravenously or orally in 22 trials demonstrated a mortality rate of 7.7% in the control group, which was reduced to 7.4% in the nitrate group. Taken together, randomized and pooled data are consistent with a possible modest treatment effect of nitrates such that 3 to 4 deaths might be prevented for every 1000 patients treated.
Dosing
The dose nitroglycerin is 0.4 mg administered sublingually. Intravenous nitroglycerin offers an advantage over sublingual administration in so far as it allows clinicians to titrate the therapy in response to the patient’s blood pressure. The usual intravenous nitroglycerin infusion rate is 5 to 10 mcg per minute with an increases of 5 to 20 mcg per minute until symptoms are relieved or mean arterial blood pressure (MAP) is reduced by 10% of its baseline level in normotensive patients and by up to 30% for hypertensive patients. In no case should the systolic blood pressure be lowered below 90 mm Hg or should the systolic blood pressure drop greater than 30 mm Hg below baseline. [4] [5]
Nitrates versus Beta-Blocker Administration
In so far as the mortality benefits of nitrates are limited, their dosing should be titrated to a blood pressure that does not limit the co-administration of beta-blockers, which have, in contrast, been associated with advantages in mortality and infarct size reduction.
Side Effects and Contraindications
The systolic blood pressure may drop rapidly following a sublingual nitroglycerine secondary to inability to control both the initial dose and rate of absorption. Nitrates in all forms should be avoided in patients with initial systolic blood pressures less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, marked bradycardia or tachycardia [6], or known or suspected right ventricular infarction. Patients with right ventricular infarction are especially dependent on adequate right ventricular preload to maintain cardiac output and may experience profound hypotension during administration of nitrates [7] Phosphodiesterase inhibitors potentiate the hypotensive effects of nitrates because of their mechanism of action in releasing nitric oxide and increasing cyclic guanosine monophosphate.[8] Therefore, it is useful clinical practice to ascertain whether such agents have been used, and nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction in the prior 24 hours (48 hours for tadalafil).
Guidelines (DO NOT EDIT)
Class I
1. Patients with ongoing ischemic discomfort should receive sublingual nitroglycerin (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous nitroglycerin. (Level of Evidence: C)
2. Intravenous nitroglycerin is indicated for relief of ongoing ischemic discomfort, control of hypertension, or management of pulmonary congestion. (Level of Evidence: C)
Class III
1. Nitrates should not be administered to patients with systolic blood pressure less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, severe bradycardia (less than 50 beats per minute [bpm]), tachycardia (more than 100 bpm), or suspected RV infarction. (Level of Evidence: C)
2. Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (48 hours for tadalafil). (Level of Evidence: B)[9]
References
- ↑ Abrams J. Hemodynamic effects of nitroglycerin and long-acting nitrates. Am Heart J 1985;110:216-24.
- ↑ Winbury MM. Redistribution of left ventricular blood flow produced by nitroglycerin: an example of integration of the macro and microcirculation. Circ Res 1971;28(Suppl 1):140-7.
- ↑ Gorman MW, [[Category:]]Sparks HV. Nitroglycerin causes vasodilatation within ischaemic myocardium. Cardiovasc Res 1980;14:515-21.
- ↑ Libby P, Braunwald's Heart Disease, 8th edition, 2007
- ↑ Fuster, O'Rourke, Walsh, Poole-Wilson, Hurst's The Heart, 12th edition, 2008
- ↑ Come PC, Pitt B. Nitroglycerin-induced severe hypotension and bradycardia in patients with acute myocardial infarction. Circulation 1976;54:624-8.
- ↑ Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 1994;330:1211-7.
- ↑ Cheitlin MD, Hutter AM, Brindis RG, et al. ACC/AHA expert consensus document on the use of sildenafil (Viagra) in patients with cardiovascular disease. American College of Cardiology/American Heart Association. J Am Coll Cardiol 1999;33:273-82.
- ↑ Antman E.M., Hant M., Armstrong P.W., et. al., 2007 Focused updates of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation published online Dec 10, 2007; DOI: 10.1161/CIRCULATION AHA.107.188209