Cardiogenic shock complicating acute myocardial infarction: The use of coronary angioplasty and the integration of the new support devices into patient management

Conventional therapy for cardiogenic shock complicating acute myocardial infarction continues to be associated with a high in-hospital mortality rate. Hemodynamic support with new mechanical devices and emergency coronary revascularization may alter the long-term prognosis for patients with this complication. Between July 1985 and March 1990, 68 patients presented to the University of Michigan with acute myocardial infarction and cardiogenic shock. Interventions performed included thrombolytic therapy (46%), intraaortic balloon pump counterpulsation (70%), cardiac catheterization (86%), coronary angioplasty (73%), emergency coronary artery bypass grafting/ventricular septal defect repair (15%), Hemopump insertion (11%), percutaneous cardiopulmonary support (4%) and ventricular assist device (3%).The 30-day survival rate was significantly better in patients who had successful angioplasty of the infarct-related artery than in patients with failed angioplasty (61% vs. 7%, p = 0.002) or no attempt at angioplasty (61% vs. 14%, p = 0.003). This difference was maintained over the 1-year follow-up period. The only clinical variable that predicted survival was age <65 years.The early use of the new support devices in 10 patients was associated with death in 8 (80%), but this poor outcome may reflect a selection bias for an especially high risk population. Collectively, these recent data continue to suggest that emergency revascularization with angioplasty may reduce the mortality rate, but further study is required to define optimal utilization and integration of new support devices

Complete atrioventricular block complicating inferior wall acute myocardial infarction treated with reperfusion therapy

Previous studies report larger myocardial infants and increased in-hospital mortality rates in patients with inferior wall acute myocardial infarction (AMI) and complete atrioventricular block (AV), but the clinical implications of these complications in patients treated with reperfusion therapy have not been addressed. The clinical course of 373 patients--50 (13%) of whom developed complete AV block--admitted with inferior wall AMI and given thrombolytic therapy within 6 hours of symptom onset was studied. Acute patency rates of the infarct artery after thrombolytic therapy were similar in patients with or without AV block. Ventricular function measured at baseline and before discharge in patients with complete AV block showed a decrement in median ejection fraction (-3.5 vs -0.4%, P = 0.03) and in median regional wall motion (-0.14 vs +0.24 standard deviations/chord, P = 0.05). The reocclusion rate was higher in patients with complete AV block (29 vs 16%, P = 0.03). Patients with complete AV block had more episodes of ventricular fibrillation or tachycardia (36 vs 14%, p &lt; 0.001), sustained hypotension (36 vs 10%, p &lt; 0.001), pulmonary edema (12 vs 4%, P = 0.02) and a higher in-hospital mortality rate (20 vs 4%, p &lt; 0.001), although the mortality rate after hospital discharge was identical (2%) in the 2 groups. Multivariable logistic regression analysis revealed that complete AV block was a strong independent predictor of in-hospital mortality (p = 0.0006). Thus, despite initial successful reperfusion, patients with inferior wall AMI and complete AV block have higher rates of in-hospital complications and mortality.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29481/1/0000567.pd

Comparison of thallium-201 SPECT redistribution patterns and rubidium-82 PET rest-stress myocardial blood flow imaging

To compare regional thallium-201 SPECT redistribution patterns with rubidium-82 PET, we studied 81 patients with both imaging modalities. Sixty patients had significant coronary artery disease. All patients underwent PET imaging after dipyridamole infusion, while SPECT imaging was performed after exercise stress (38 patients) and dipyridamole (43 patients). Sixty-eight percent of patients with prior infarct had fixed defects on SPECT, compared to 39% with PET. Sixty-one percent of patients with prior infarct had PET perfusion defects which exhibited ‘reflow’ or normal rubidium-82 tracer uptake (p < 0.05 vs. SPECT). Similar results were seen in patients without prior infarct (26% fixed defects on SPECT vs. 12% for PET, p < 0.05). Regional analysis showed that 57% of fixed SPECT defects corresponded to PET defects with reflow or normal rubidium-82 uptake, while 78% of ‘fixed’ PET defects corresponded to fixed SPECT defects. PET reflow and normal rubidium-82 uptake in sites of fixed thallium-201 SPECT perfusion defects suggest that imaging modalities employing separate tracer injections at rest and after stress, such as rubidium-82 PET, may be more specific in the assessment of myocardial viability, especially in patients with prior myocardial infarction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42537/1/10554_2005_Article_BF01151577.pd

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.