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PubMed2006

Plaque volume and occurrence and location of periprocedural myocardial necrosis after percutaneous coronary intervention: insights from delayed-enhancement magnetic resonance imaging, thrombolysis in myocardial infarction myocardial perfusion grade analysis, and intravascular ultrasound.

BACKGROUND: Myocardial necrosis can occur during percutaneous coronary intervention (PCI) despite optimal adjunctive pharmacology and careful technique. We investigated the mechanisms of procedural infarction using angiographic analysis, intravascular ultrasound, and delayed-enhancement magnetic resonance imaging. METHODS AND RESULTS: Fifty-two patients (64 vessels) who underwent complex PCI were studied. All patients were preloaded with clopidogrel and received glycoprotein IIb/IIIa inhibitors. "Adjacent" myonecrosis was defined as the presence of an area of new gadolinium hyperenhancement close to the stent. "Distal" myonecrosis was defined as situated at least 10 mm downstream from the stent. Fifteen vessels (23%) had evidence of new hyperenhancement after PCI. Of these, 8 (12%) had the distal type, and 7 (11%) had the adjacent type. Intravascular ultrasound showed a significantly greater reduction in plaque volume (91.6+/-51.5 versus 8+/-14 versus 20+/-35 mm3; P < 0.001) in the group with distal hyperenhancement compared with patients without new hyperenhancement or adjacent hyperenhancement. In the entire sample, a significant correlation was seen between changes in plaque volume (rho = 0.58, P < 0.001) after PCI and the mass of new necrosis measured by magnetic resonance imaging. Thrombolysis in Myocardial Infarction perfusion grade assessment of a closed microvasculature after PCI carried an odds ratio of 8.0 (95% confidence interval, 1.4 to 46.1; P = 0.02) for the occurrence of hyperenhancement, whereas side-branch occlusion was associated with an odds ratio of 16.2 (95% confidence interval, 2.6 to 102.5; P = 0.03). However, a closed microvasculature was associated with distal hyperenhancement (P = 0.02), and side-branch occlusion was associated with adjacent hyperenhancement (P < 0.001). CONCLUSIONS: These data suggest that distal embolization of plaque material occurs in contemporary PCI of native coronary arteries. Efforts to minimize procedural necrosis may require careful review of side branch anatomy and/or use of distal protection during extensive coronary stenting.

Aged↗
PubMed1991

[Non-Q wave myocardial infarction. Recurrent myocardial infarction, unstable angina and arrhythmia in 8-year observation].

UNLABELLED: The contradictory views on long term clinical course of patients after non-Q wave myocardial infarction (NQMI) as compared with those after Q wave myocardial infarction (QMI)--induced us to undertake a comparative study of both types of myocardial infarction during a 8 year follow-up. The study was carried out in 400 patients (pts) with NQMI (mean age 51) and 485 pts with QMI (mean age 53). Both groups were compared. We have analysed the following parameters: the dynamics of ischaemic heart disease (unstable angina, reinfarction, arrhythmias, mortality) and coronary arteriography. During 8 year observation unstable angina and arrhythmias, were statistically more frequent in pts after NQMI. Recurrent myocardial infarction occurred in 196 (49%) of pts after NQMI and only in 87 pts (18%) after QMI (p less than 0.001). However, the difference in mortality between both groups was not significant (37% vs 39% respectively). Coronary angiography was performed at 1-6 months after myocardial infarction. In 65% of pts after NQMI detected lesions were limited to proximal part of one or two coronary arteries. CONCLUSION: NQMI is characterized by unstable long-term clinical course, and that is why pts with NQMI should be recommended for early coronary angiography and revascularization.

Adult↗
PubMed2002

Development and validation of a short measure of health status for individuals with acute myocardial infarction: the myocardial infarction dimensional assessment scale (MIDAS).

The purpose of this study was to develop and validate a disease-specific health status measure for individuals with myocardial infarction (MI). The development of the myocardial infarction dimensional assessment scale (MIDAS) followed three main stages. Stage 1 consisted of in-depth, semi-structured, exploratory interviews conducted on a sample of 31 patients to identify areas of salience and concern to patients with MI. These interviews generated 48 candidate questions. In stage 2 the 48-item questionnaire was used in a postal survey to identify appropriate rephrasing/shortening, to determine acceptability and to help identify sub-scales of the instrument addressing different dimensions of MI. Finally, in stage 3 the construct validity of MIDAS subscales was examined in relation to clinical and other health outcomes. A single centre (district general hospital) in England was used for stages 1 and 3 and a national postal survey was conducted for stage 2. A total of 410 patients were recruited for the national survey (stage 2). Full data were available on 348 (85%) patients. One hundred and fifty-five patients were recruited to test construct validity (stage 3). The MIDAS contains 35 questions measuring seven areas of health status: physical activity, insecurity, emotional reaction, dependency, diet, concerns over medication and side effects. The measure has high face, internal and construct validity and is likely to prove useful in the evaluation of treatment regimes for MI.

Activities of Daily Living↗
PubMed1981

[Stress-ECG after myocardial infarct. Does myocardial infarct reduce the significance of stress ECG in the diagnosis of severe stenosis of the anterior interventricular ramus, the diagonal ramus and the marginal ramus of the coronary artery].

41 patients with inferior myocardial infarction underwent both exercise stress testing and coronary arteriography. Coronary arteriography of 15 patients showed high-degree stenosis as well as occlusions of the right coronary artery and/or of the R. circumflexus of the left coronary artery alone. In 14 of these 15 cases exercise stress testing showed a normal result, in one case results were abnormal. However, we detected additional high-degree stenosis of R. interventricularis anterior and/or of R. diagonalis and/or of R. marginalis in the other 26 patients. In 22 of these 26 cases exercise stress testing showed an abnormal result, in 4 cases it was normal. Because of a sensitivy of 84,6% and a specificity of 93,3% we can assume, that abnormal results of exercise stress testing suggest additional high-degree stenosis of the RIVA-vessel system in patient after inferior myocardial infarction. Considering an eventual bypass operation it is possible to narrow the indication for coronary arteriography.

Adult↗
PubMed1995

Outcomes in African-American women with suspected acute myocardial infarction: the Myocardial Infarction Triage and Intervention Project.

Increasing attention has been given to the investigation of cardiovascular disease in women, although African-American women have received little attention. This study compares characteristics and outcomes in women admitted to coronary care units for suspected acute myocardial infarction (MI). Between January 1988 and December 1991, a total of 554 (5%) African-American and 9738 (95%) white women with suspected acute MI were admitted to coronary care units in metropolitan Seattle, Washington. Relevant demographic socioeconomic, clinical, and outcome data were abstracted from the medical record and entered in the Myocardial Infarction Triage and Intervention registry. African-American women were younger, more often single and unemployed, and were less likely to have health insurance than their white counterparts. In addition, a higher proportion of African-American women reported a history of hypertension and diabetes mellitus. After adjustment for age, African-American women were equally as likely to develop acute MI and were more likely to die in the hospital. In addition, a higher proportion of African-American women were readmitted to coronary care units for suspected MI. Compared with their white counterparts, African-American women with suspected acute MI were considerably worse off from both socioeconomic and clinical standpoints, and their relative disadvantage was apparent in poor outcomes.

Black or African American↗
PubMed1997

Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial infarction Study Group.

BACKGROUND: A simple clinical method to stratify risk for patients who have had successful reperfusion therapy after myocardial infarction is attractive since it facilitates the tailoring of therapy. METHODS: We investigated the clinical value of the 12-lead electrocardiogram (ECG), in 403 patients after successful reperfusion therapy by primary coronary angioplasty, in relation to infarct size measured by enzyme activity, left-ventricular function, and clinical outcome. ECGs were analysed to find the extent of the ST-segment-elevation resolution 1 h after reperfusion therapy. FINDINGS: A normalised ST segment was seen in 51% of patients, a partly normalised ST segment in 34%, and 15% had no ST-segment-elevation resolution. Enzymatic infarct size and ejection fraction were related to the extent of the early resolution of the ST segment. The relative risk of death among patients with no resolution compared with patients with a normalised ST segment was 8.7 (95% CI 3.7-20.1), and that among patients with partial resolution compared with patients with a normalised ST segment was 3.6 (1.6-8.3). INTERPRETATION: Our findings suggest that ECG patterns reflect the effectiveness of myocardial reperfusion. Patients for whom reperfusion therapy by primary angioplasty was successful and who had normalised ST segments had limited damage to the myocardium and an excellent outlook during follow-up. Patients with persistent ST elevation after reperfusion therapy may need additional interventions since they have more extensive myocardial damage and have a higher mortality rate.

Aged↗
PubMed2001

Double-blind, randomized trial of an anti-CD18 antibody in conjunction with recombinant tissue plasminogen activator for acute myocardial infarction: limitation of myocardial infarction following thrombolysis in acute myocardial infarction (LIMIT AMI) study.

BACKGROUND: Inhibition of leukocyte adhesion can reduce myocardial infarct size in animals. This study was designed to define the safety and efficacy of a recombinant, humanized, monoclonal antibody to the CD18 subunit of the beta2 integrin adhesion receptors (rhuMAb CD18), in reducing infarct size in patients treated with a thrombolytic agent. METHODS AND RESULTS: The Limitation of Myocardial Infarction following Thrombolysis in Acute Myocardial Infarction Study (LIMIT AMI) was a randomized, double-blind, placebo-controlled, multicenter study conducted in 60 centers in the United States and Canada. A total of 394 subjects who presented within 12 hours of symptom onset with ECG findings (ST-segment elevation) consistent with AMI were treated with recombinant tissue plasminogen activator and were also given an intravenous bolus of 0.5 or 2.0 mg/kg rhuMAb CD18 or placebo. Coronary angiography was performed at 90 minutes, 12-lead ECGs were obtained at baseline, 90, and 180 minutes, and resting sestamibi scans were performed at >/=120 hours. Adjunctive angioplasty and use of glycoprotein IIb/IIIa antiplatelet agents at the time of angiography were discretionary. There were no treatment effects on coronary blood flow, infarct size, or the rate of ECG ST-segment elevation resolution, despite the expected induction of peripheral leukocytosis. A slight trend toward an increase in bacterial infections was observed with rhuMAb CD18 (P=0.33). CONCLUSIONS: RhuMAb CD18 was well tolerated but not effective in modifying cardiac end points.

Antibodies, Monoclonal↗
PubMed1975

Surgery for impending myocardial infarction, acute evolving myocardial infarction, and complications of myocardial infarction.

Post-infarction ventricular aneurysm, ventricular septal defect, and mitral insufficiency are all potentially amenable to surgical intervention. In each instance the results of operation and the prognosis following operation depend largely on the extent of infarction, the status of the residual myocardium, and the interval between infarction and operation. When the residual myocardium exhibits good contractility, the results are usually good. When early operation is performed in the face of a deteriorating clinical course and with poorly contracting residual myocardium, the mortality rates are extremely high. In an effort to increase the efficiency of the residual myocardium, concomitant coronary bypass surgery should be performed whenever possible. In this difficult group, more recent supportive measures such as the intra-aortic balloon pump may be particularly helpful when utilized both before and after operation. The surgical indications and results of coronary bypass surgery in impending or acute evolving myocardial infarction are not as well defined, but it is evident that myocardial revascularization may be useful in carefully selected patients.

Acute Disease↗
PubMed1993

Subacute ventricular free wall rupture complicating myocardial infarction.

Myocardial free wall rupture accounts for between 8% and 17% of mortality after myocardial infarction. In up to 40% of cases death occurs subacutely over a matter of hours, not minutes. Illustrative clinical cases and data suggest that a high degree of clinical suspicion, along with the early use of echocardiography, could significantly reduce mortality resulting from myocardial free wall rupture complicating myocardial infarction. Myocardial free wall rupture should be suspected in patients with recent myocardial infarction who have recurrent or persistent chest pain, hemodynamic instability, syncope, pericardial tamponade, or transient electromechanical dissociation. In this clinical situation, emergent echocardiography showing a pericardial effusion or pericardial thrombus is highly suggestive of free wall rupture. Surgical exploration and rupture repair is the definitive diagnostic and therapeutic procedure.

Aged↗
PubMed2002

Cyclooxygenase-2 in myocardium stimulation by angiotensin-II in cultured cardiac fibroblasts and role at acute myocardial infarction.

Myocardial infarction is followed by a complex repair process that includes a significant role for inflammatory cells. Cyclooxygenase-2 (COX-2) plays a key role in mediating inflammation. Contribution of COX-2 to inflammatory response following myocardial infarction is less certain. In an effort to evaluate the function of COX-2 and prostaglandin E(2)(PGE(2)) in myocardial infarction, we examined the role of COX-2 after angiotensin II (Ang II) stimulation in cardiac fibroblasts and in rats with experimental myocardial infarction (MI). We combined Western blot analysis and enzyme immunoassay to demonstrate COX-2 expression and PGE(2)release in cardiac fibroblasts. Isolated cardiac fibroblasts were stimulated with Ang II. Unstimulated fibroblasts showed no COX-2 protein expression. Fibroblasts stimulated with Ang II showed a strong time-dependent expression of COX-2 protein. The p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 but not the p42/44 MAPK-inhibitor PD98059 suppressed Ang II-induced COX-2 protein expression. COX-2 expression correlated with a significantly increased PGE(2)release from cardiac fibroblasts. The COX-2 specific inhibitor NS-398 suppressed the Ang II-stimulated PGE(2)production. We then investigated COX-2 expression and inflammatory cell infiltration in our rat model of myocardial infarction. MI was produced by coronary artery ligation in adult female Wistar rats. The period of coronary artery occlusion was 96 h. The selective COX-2 inhibitor rofecoxib (3 mg/kg/d), administered orally, was given one day before MI and continued for four days. Western blotting showed expression of COX-2 protein in the area of necrosis and the infarct border zone. Immunofluorescence analysis showed macrophage infiltration as well as fibroblast proliferation in the infarct border zone of 4-d infarcted tissue and a significantly reduced cell invasion and fibroblast proliferation in infarcted tissue of rats treated with rofecoxib. MI size at day 4 was comparable in untreated and treated rats. In conclusion, we demonstrate that pharmacological interference with prostaglandin synthesis in myocardial infarction is associated with reduced myocardial invasion of inflammatory cells.

Angiotensin II↗