Rate Of Recurrent Infarction Research Articles

Abstract 79: Mechanisms of Early Recurrence in Intracranial Atherosclerotic Disease (MyRIAD) Study: Participants, Clinical and Imaging Outcomes

Introduction: ICAD is a common cause of stroke. MyRIAD is designed to identify mechanisms of ischemia and predictors of recurrence in ICAD. Here we present the study population baseline characteristics and key outcomes. Methods: MyRIAD is an NIH/NINDS funded prospective multicenter observational study of patients with recent ( < 21 days) stroke or TIA (recurrent or with DWI) caused by IAD 50-99% without planned angioplasty/stenting. The primary outcome is ischemic stroke in the territory within 1 year of follow up; secondary outcomes are TIA at 1 year and new infarcts on MRI at 6-8 weeks. Qualifying events and clinical and imaging outcomes are centrally adjudicated. Results: MyRIAD enrolled 105 participants. The MyRIAD cohort (Table) had significant atherosclerotic risk factors and received aggressive medical therapy. Of 101 participants with clinical follow up (mean 243 + 126 days), the primary outcome of stroke in the territory at 1 year occurred in 9 (8.6%, 13.4/100 person-years), while 7 (6.7%, 10.4/100 person-years) had a TIA. A study MRI at 6-8 weeks was available for comparison to baseline MRI in 87 participants (mean time from qualifying event to follow up imaging 51 + 16 days). A new DWI/FLAIR infarct in the territory of the symptomatic vessel was noted in 22 participants (25.3%). Conclusions: MyRIAD detected an 8.6% 1-year stroke recurrence and a much higher 25.3% rate of recurrent infarction in the first weeks after qualifying stroke/TIA, emphasizing the need to develop better therapeutic interventions for ICAD.

One-Year Outcomes after PCI Strategies in Cardiogenic Shock

BackgroundAmong patients with acute myocardial infarction, cardiogenic shock, and multivessel coronary artery disease, the risk of a composite of death from any cause or severe renal failure leading to renal-replacement therapy at 30 days was found to be lower with percutaneous coronary intervention (PCI) of the culprit lesion only than with immediate multivessel PCI. We evaluated clinical outcomes at 1 year.MethodsWe randomly assigned 706 patients to either culprit-lesion-only PCI or immediate multivessel PCI. The results for the primary end point of death or renal-replacement therapy at 30 days have been reported previously. Prespecified secondary end points at 1 year included death from any cause, recurrent myocardial infarction, repeat revascularization, rehospitalization for congestive heart failure, the composite of death or recurrent infarction, and the composite of death, recurrent infarction, or rehospitalization for heart failure.ResultsAs reported previously, at 30 days, the primary end point had occurred in 45.9% of the patients in the culprit-lesion-only PCI group and in 55.4% in the multivessel PCI group (P=0.01). At 1 year, death had occurred in 172 of 344 patients (50.0%) in the culprit-lesion-only PCI group and in 194 of 341 patients (56.9%) in the multivessel PCI group (relative risk, 0.88; 95% confidence interval [CI], 0.76 to 1.01). The rate of recurrent infarction was 1.7% with culprit-lesion-only PCI and 2.1% with multivessel PCI (relative risk, 0.85; 95% CI, 0.29 to 2.50), and the rate of a composite of death or recurrent infarction was 50.9% and 58.4%, respectively (relative risk, 0.87; 95% CI, 0.76 to 1.00). Repeat revascularization occurred more frequently with culprit-lesion-only PCI than with multivessel PCI (in 32.3% of the patients vs. 9.4%; relative risk, 3.44; 95% CI, 2.39 to 4.95), as did rehospitalization for heart failure (5.2% vs. 1.2%; relative risk, 4.46; 95% CI, 1.53 to 13.04).ConclusionsAmong patients with acute myocardial infarction and cardiogenic shock, the risk of death or renal-replacement therapy at 30 days was lower with culprit-lesion-only PCI than with immediate multivessel PCI, and mortality did not differ significantly between the two groups at 1 year of follow-up. (Funded by the European Union Seventh Framework Program and others; CULPRIT-SHOCK ClinicalTrials.gov number, NCT01927549.)

Heparin in Acute Myocardial Infarction

Thrombolytic therapy has become an established procedure in patients with acute myocardial infarction (AMI). However, the aftercare of such patients is still uncertain. A meta-analysis of twenty trials of intravenous or subcutaneous heparin in AMI performed during the prethrombolysis period indicated a significant reduction in mortality, reinfarction, and stroke in treated patients. More recently, a study (SCATI) aimed at investigating the clinical effects of subcutaneous heparin (12.500 U two times daily) in the setting of thrombolytic therapeutical strategy in AMI, showed a lower in-hospital mortality, a trend towards lesser transient ischemic episodes in patients given streptokinase, and no difference in recurrent infarction rate. Ventricular thrombi were markedly reduced by heparin. Anti-platelet drugs were not permitted in the SCATI. In both GISSI 2 (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico) and International tissue plasminogen activator/streptokinase trials, aspirin was a recommended treatment, and subcutaneous heparin was randomized. No difference in mortality was noted in patients given heparin. In GISSI 2 recurrent ischemic episodes were also similar in treated and control groups, whereas embolic events were reduced by heparin. Major bleedings were rare in all trials. In conclusion, subcutaneous heparin is beneficial in AMI: however, the association with aspirin does not add consistent benefits. Heparin is effective in preventing thrombus formation and embolic complications - such effects are not shared by aspirin.

Uncomplicated Acute Myocardial Infarction

The natural history of uncomplicated acute myocardial infarction has not been well defined. One hundred eighty-eight patients younger than 65 years who survived an uncomplicated acute myocardial infarction were mobilized rapidly, underwent symptom-limited exercise testing for an average of 10.7 days, returned to work at an average of 6.7 weeks, and were observed either until death or 5 years after the acute infarction. Twenty-two (12%) patients have died of cardiac causes and 46 (25 %) have had recurrent infarctions, fatal or nonfatal, 5 years after the index event. The death and recurrent infarction rates were higher at 6 months than at 5 years after the initial attack. Recurrent infarction or death at 6 months was predicted by a history of effort angina preceding the initial infarction. At 5 years the only predictive variable was radiological cardiomegaly, which was predictive of nonfatal reinfarction. Exercise test variables predicted neither death nor reinfarction; however, exercise test angina did predict post-infarction angina pectoris or coronary bypass surgery (P < .02). The chance of death or reinfarction at 6 months, cardiac death at 5 years, and the occurrence of late angina or coronary bypass surgery (P < .05), increased the later the exercise test was performed after myocardial infarction. In this carefully selected group, 5-year survival rate and status were surprisingly good, were not adversely affected by the vigorous management, and the outcome was as well predicted by the timing of exercise testing as any of the more formal clinical and exercise test variables measured.