Acute myocardial infarction prognosis

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Goldberg RJ, Zevallos JC, Yarzebski J, et al. Prognosis of acute myocardial infarction complicated by complete heart block (the Worcester Heart Attack Study). Am. J. Cardiol. 1992 69 1135-41. 

Measurements of arterial pressure, cardiac output, stroke work index, and pulmonary capillary wedge pressure are particularly useful in patients with acute myocardial infarction and acute heart failure. Such patients can be usefully characterized on the basis of three hemodynamic measurements arterial pressure, left ventricular filling pressure, and cardiac index. One such classification and therapies that have proved most effective are set forth in Table 13-4. When filling pressure is greater than 15 mm Hg and stroke work index is less than 20 g-m/m2, the mortality rate is high. Intermediate levels of these two variables imply a much better prognosis. 

O Connor CM, Califf RM, Massey EW, et al. Stroke and acute myocardial infarction in the thrombolytic era clinical correlates and long-term prognosis. J Am Coll Cardiol. 1990 16 533-540. 

In another study of 45 patients with ACS, the relationship between plaque rupture, CRR and prognosis was investigated with intravascular ultrasound (21). These 45 patients had a first acute myocardial infarction with or without ST segment elevation. Intravascular ultrasound was performed in the patients before any percutaneous coronary intervention and within six hours of symptoms (21). The remaining coronary vasculature was examined within one month. Forty-five culprit arteries and 84 other coronary arteries were examined with intravascular ultrasound. They found that plaque ruptures in 47% of the arteries at the culprit site in the acute phase of the myocardial infarction. In addition, intravascular ultrasound revealed 17 occult plaque ruptures at remote sites in 24% of the patients (21), These findings suggest that some patients with acute myocardial infarctions have multiple plaque ruptures in other coronary arteries and the culprit artery. 

Decreased reperfusion at the microvascular level might also contribute to the poorer prognosis of diabetic patients. Recent work in acute myocardial infarction (Ml) has suggested that despite achieving comparable rates of thrombosis in myocardial infarction (TIMI)-3 flow, diabetics have poorer post-PCI myocardial reperfusion than nondiabetics, as evidenced by reduced ST-segment resolution and myocardial blush grade (15). 

More trials during and after myocardial infarction have been pubhshed and subjected to meta-analysis (12). This very large database provides valuable information on the rate of the most common adverse effects. Of all trials of the effects of ACE inhibitors on mortality in acute myocardial infarction, only the CONSENSUS II trial did not show a positive effect. In this trial, enalaprUat was infused within 24 hours after the onset of symptoms, followed by oral enalapril. The reasons for the negative result of CONSENSUS II remain unresolved, but hypotension and a proischemic effect linked to a poorer prognosis have been suggested. 

M. Ishihara, H. Sato, H. Tateishi, T. Kawagoe, Y. Shimatani, S. Kurisu, K. Sakai, K. Ucda, Implications of prodromal angina pectoris in anterior Wall acute myocardial infarction acute angiographic findings and long-term prognosis, J Am Coll Cardiol 31, 1701 (1998). 

Finally, the development of a bifascicular block (RBBB plus SAH, or RBBB plus inferoposterior hemiblock (IPH)) during the acute myocardial infarction usually is considered a poor prognosis, since this is indicative of a large infarction and the involvement of, at least, two territories (LAD and RCA or LCX). However, on the basis of HERO-2 trial, no data (Wong et al., 2006a) have been found showing that there was no difference in 30-day mortality. 

Anteroseptal versus inferolateral MI prognostic implications. It is known that the MI involving LAD presents for similar area of necrosis, increased myonecrosis, reduced early and late left-ventricular function and high mortality compared with infarction in other vascular territories. However, the mechanisms underlying a worse prognosis are not completely characterised. Recently, it has been demonstrated (Kandzari et al, 2006) that prognosis after primary PCI in patient with ACS, the majority with ST-segment elevation, is different in patients with LAD occlusion than in RCA or LCX. Acute myocardial infarction due to LAD is associ-... 

Corbalan R, Prieto JC, Chavez E, Nazzal C, Cumsille F, Krucoff M. Bedside markers of coronary artery patency and shortterm prognosis of patients with acute myocardial infarction and thrombolysis. Am Heart J 1999 138 533. 

Jacobs DR, Jr, Kroenke C, Crow R et al. PREDICT a simple risk score for clinical severity and long-term prognosis after hospitalization for acute myocardial infarction or unstable angina the Minnesota heart survey. Circulation 1999 100(6) 599-607. 

Schwartz PJ, Zaza A, Grazi S et al. Effect of ventricular fibrillation complicating acute myocardial infarction on longterm prognosis importance of the site of infarction. Am J Cardiol 1985 56 384. 

Zairis MN, Manousakis SJ, Stefanidis AS et al. C-reactive protein levels on admission are associated with response to thrombolysis and prognosis after ST-segment elevation acute myocardial infarction. Am Heart J 2002 144 782. 

Boden WE, van Gilst WH, Scheldewaert RG, et al. Diltiazem in acute myocardial infarction treated with thrombolytic agents A randomised, placebo-controlled trial. Incomplete Infarction Trial of European Research Collaborators Evaluating Prognosis post-Thrombolysis (INTERCEPT). Lancet 2000 355 1751-1756. 

In addition to assessing prognosis in stable patients, nuclear perfusion imaging has been used in a prospective manner to help risk-stratify survivors of acute myocardial infarction. Mahmarian et al. (33) used the extent of total and ischemic perfusion defect size (PDS) on adenosine " Technetium sestamibi scans to stratify patients into low-, middle-, and high-risk groups, with... 

Type I second-degree AV block with bundle branch block (which is far less common than narrow QRS type I block) must not be automatically labeled as AV nodal. Outside of acute myocardial infarction, type I block and bundle branch block (QRS > 0.12 s) occur in the His-Purkinje system in 60-70% of the cases (10) (Fig. 10.5). In such cases exercise is likely to aggravate the degree of AV block. Yet, many still believe that type I blocks are all AV nodal and therefore basically benign. It is believed that the prognosis of infranodal type I block is as serious as that of type II block and a permanent pacemaker... 

In the acute setting of cocaine-induced chest pain, assessment includes the possible diagnosis of acute myocardial infarction. However, cocaine may independently affect cardiac biomarkers [22 ]. Recent cocaine use may alter the specificity of measurement of serum creatine kinase and its MB Iraction. Among cocaine users, increased serum creatine kinase activities and increased mean myoglobin concentrations are common. Increased skeletal muscle activity and rhab-domyolysis are often present, possibly because of cocaine-induced hyperthermia. Troponin I concentrations are more reliable cardiac biomarkers for detecting cocaine-induced myocardial infarction and are associated with a poor prognosis. 

Lamfers EJ, Hooghoudt TE, Herzberger DP, Schut A, Stol-wijk PW, Verheugt FW. Abortion of acute ST segment elevation myocardial infarction after reperfusion incidence, 6 kifeiie characteristics and prognosis. Heart 2003 89 496. 

Ironically, patients are frequently referred after a cardiac arrest when the etiology is clearly transient or due to correctable ischemia. In either case, an ICD alone will not improve the prognosis. A patient who has an ischemic cardiac arrest due to a left main lesion in the face of normal ventricular function will not derive substantial benefit from an ICD alone. An ICD may be of no benefit for a patient who has ventricular fibrillation or cardiac arrest due to an acute Q wave myocardial infarction. 

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