Evidence-based use of nitro?

[zzyzx]

From what the latest AHA guidelines say, only ASA has been proven to reduce mortality for patients suffering MI's. Is it really true that there are no studies that have proven the effectiveness of nitro? Are we just using just because that's what we've always done and because there seems to be an explanation for how it can work in reducing the size of an infarct?

[firefighter523]

Nitro only delays the inevitable, nitro is NOT the fix for MIs, A STENT IS! Google studies on stents, you might find what you are looking for.

[ERDoc]

Nitro only delays the inevitable, nitro is NOT the fix for MIs, A STENT IS! Google studies on stents, you might find what you are looking for.

And your evidence to support this statement is?

[AnthonyM83]

Google studies on stents, you might find what you are looking for.

He's looking for evidence for use of nitro...not stents or what helps MIs survive....

[brock8024]

Nitro helps vasodilate coronary arteries, which in return, supples the heart muscle with oxygen which helps lessen damage to the heart muscle. I might be wrong but how could this not help the heart during a AMI. This is why we use MONA. We try at every angle to help the heart muscle til a stent or what ever needs to be done.

[AnthonyM83]

Right, it makes great sense in theory...but he's saying AHA apparently believes there's been no evidence to support nitro reducing mortality. So, anyone have evidence?

[AZCEP]

Protection of ischemic myocardium by nitroglycerin: experimental and clinical results.

Epstein SE, Borer JS, Kent KM, Redwood DR, Goldstein RE, Levitt B.

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.

PMID: 815059 [PubMed - indexed for MEDLINE]

So apparently, we use NTG to reduce the size of the injured tissue, which helps to limit the amount of myocardium that dies (infarcts). We are also helping to preserve cardiac function by reducing the preload into the left ventricle, reducing the workload.

[AZCEP]

Hemodynamic effects of nitroglycerin in acute myocardial infarction

DO Williams, EA Amsterdam and DT Mason

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agnet in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (less than or equal to 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (greater than 12 MM Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 TO 7 MM Hg; P less than .01), mean systemic arterial pressure (MAP) (95 TO 82 MM Hg; P less than .01), cardiac index (CI) (1.79 TO 1.46 L/min/m-2; P less than .02), stroke index (SI) (24 TO 18 CC/M-2; P less than .01) and stroke work index (SWI) (27 TO 20 GM TIMES M/M-2; P less than .01). These alterations were significant in both subgroups, with the decline in PAW greater (P less than .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline ofpump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accomppanied by potentially deleterious fall in cardiac output and systemic blood pressure.

[Dustdevil]

Hemodynamic effects of nitroglycerin in acute myocardial infarction

DO Williams, EA Amsterdam and DT Mason...

So apparently, we use NTG to reduce the size of the injured tissue, which helps to limit the amount of myocardium that dies (infarcts). We are also helping to preserve cardiac function by reducing the preload into the left ventricle, reducing the workload.

[AnthonyM83]

Dust, I rarely miss a beat when people say even the most extreme things, but you definitely get the price for most "Oh, sh**, did he really just post that!?" outbursts from readers.