"No culprit" ST-elevation myocardial infarction: role of cardiac magnetic resonance imaging.

Patients with presumed ST-elevation myocardial infarction (STEMI) have no clear culprit artery in approximately 10-15% of cases. We examined the value of cardiac magnetic resonance (CMR) for diagnosis in patients with "no culprit" STEMI. Data from a comprehensive prospective registry of STEMI patients were reviewed from March 2003 to December 2009. "No culprit" patients were followed for diagnosis and clinical outcome. CMR was performed at the discretion of the attending cardiologist. Of 2728 consecutive presumed STEMI patients, 412 (15%) had no clear culprit artery. Of these, 202 (49%) had abnormal cardiac biomarkers with a definitive diagnosis in 157 (78%). Diagnoses in this group included myocardial infarction without a culprit lesion (24%), myopericarditis (22%), and stress cardiomyopathy (21%). In 210 (51%) patients with normal biomarkers, only 84 (40%) received a definitive diagnosis. Diagnoses in this group included myopericarditis (27%), noncardiac causes (21%), and cardiomyopathy (14%). CMR was performed in 123 (30%) "no culprit" patients. Patients who had CMR were more likely to have a definitive diagnosis than those who did not (95/123 [77%] vs. 144/289 [50%]; P=0.01). In particular, "no culprit" patients with abnormal biomarkers were more likely to have a definitive diagnosis with CMR. CMR led to a diagnosis different from the presumptive clinical diagnosis in 53% of all cases. CMR is a valuable diagnostic tool to improve diagnostic accuracy in patients with "no culprit" STEMI.

Treatment of refractory angina in patients not suitable for revascularization.

A growing number of patients, particularly those with advanced, chronic coronary artery disease, experience symptoms of angina that are refractory to treatment with ß-blockers, calcium-channel blockers, and long-acting nitrates, despite revascularization. The management of patients with refractory angina who are unsuitable for further revascularization is strikingly different across the world, and is contingent on local resources and available expertise. Mortality in this patient population has decreased, but enhancing quality of life remains a challenge. New treatment principles are emerging in current practice, such as metabolic modulation, therapeutic angiogenesis, and novel interventional techniques (coronary in-flow redistribution and approaches to chronic total occlusion). The contemporary management of refractory angina encourages individualized, patient-centred care in interdisciplinary, specialized clinics. Global initiatives are required to address complex clinical problem-solving for patients with refractory angina. In this Review, we discuss the epidemiology of refractory angina, and provide an update on the pharmacological, noninvasive, and interventional options that are available to these patients or are under development.

Long-term survival in patients with refractory angina.

AIMS: An increasing number of patients with severe coronary artery disease (CAD) are not candidates for traditional revascularization and experience angina in spite of excellent medical therapy. Despite limited data regarding the natural history and predictors of adverse outcome, these patients have been considered at high risk for early mortality. METHODS AND RESULTS: The OPtions In Myocardial Ischemic Syndrome Therapy (OPTIMIST) program at the Minneapolis Heart Institute offers traditional and investigational therapies for patients with refractory angina. A prospective clinical database includes detailed baseline and yearly follow-up information. Death status and cause were determined using the Social Security Death Index, clinical data, and death certificates. Time to death was analysed using survival analysis methods. For 1200 patients, the mean age was 63.5 years (77.5% male) with 72.4% having prior coronary artery bypass grafting, 74.4% prior percutaneous coronary intervention, 72.6% prior myocardial infarction, 78.3% 3-vessel CAD, 23.0% moderate-to-severe left-ventricular (LV) dysfunction, and 32.6% congestive heart failure (CHF). Overall, 241 patients died (20.1%: 71.8% cardiovascular) during a median follow-up 5.1 years (range 0-16, 14.7% over 9). By Kaplan-Meier analysis, mortality was 3.9% (95% CI 2.8-5.0) at 1 year and 28.4% (95% CI 24.9-32.0) at 9 years. Multivariate predictors of all-cause mortality were baseline age, diabetes, angina class, chronic kidney disease, LV dysfunction, and CHF. CONCLUSION: Long-term mortality in patients with refractory angina is lower than previously reported. Therapeutic options for this distinct and growing group of patients should focus on angina relief and improved quality of life.

Patients with coronary artery disease not amenable to traditional revascularization: prevalence and 3-year mortality.

OBJECTIVES: To determine the contemporary prevalence of and mortality in patients with coronary artery disease (CAD) not amenable to revascularization. BACKGROUND: A growing number of patients have severe CAD with ongoing angina despite optimal medical therapy which is not amenable to traditional revascularization. Limited data exist on contemporary prevalence and outcome for these patients. METHODS: Clinical and angiographic data were reviewed for 493 consecutive patients undergoing coronary angiography and revascularization if indicated. Patients were categorized into six groups: (1) normal coronary arteries, (2) CAD <70%, (3) CAD >70% with complete revascularization by percutaneous intervention or coronary artery bypass grafting, (4) CAD >70% with partial revascularization, (5) CAD >70% treated medically, and (6) CAD >70% on optimal medical therapy with no revascularization option. All-cause mortality at 3 years was determined. RESULTS: Prevalence for groups 1-6 was 14.8, 19.5, 36.9, 12.8, 9.3, and 6.7%, respectively. Three-year mortality increased with angiographic severity of CAD: 2.7, 6.3, 8.2, 12.7, 17.4, and 15.2%, respectively. Patients with incomplete revascularization (groups 4-6, n = 142) had higher mortality than completely revascularized patients (groups 1-3, n = 351): 14.8 vs. 6.6% (P = 0.004). CONCLUSIONS: In a contemporary series of patients undergoing coronary angiography, 28.8% (142/493) of patients had significant CAD and did not undergo complete revascularization, including 12.8% partially revascularized, 9.3% managed medically, and 6.7% with "no-option." These patients had higher mortality at 3 years (14.8 vs. 6.6%, P = 0.004) when compared with completely revascularized patients.

The efficacy and safety of enhanced external counterpulsation in patients with peripheral arterial disease.

Peripheral arterial disease (PAD) is common in patients with severe coronary artery disease (CAD) and is considered a relative contraindication to external enhanced counterpulsation (EECP), but there are no data that define the efficacy and safety of EECP in patients with PAD. The International EECP Patient Registry (IEPR) was used to compare initial post-therapy and 2-year follow-up clinical outcomes and adverse event rates in patients with and without PAD. From January 2002 to October 2004, 2126 patients were enrolled in the IEPR, of whom 493 (23%) had a history of PAD. Immediately following EECP, the reduction in angina (> or = 1 Canadian Cardiovascular Society class) was similar in patients with and without PAD (76.6% vs 79.0%, p = 0.27) as was improvement in the Duke Activity Score Index (DASI) score (+4.7% vs +6.1%, p < 0.001). Both angina reduction and DASI score improvement were sustained at 2 years. PAD patients discontinued EECP more frequently (12.0% vs 8.5%, p < 0.05), but lower extremity ulceration did not occur more frequently in patients with PAD (3.7% vs 2.7%, p = 0.26). Rates of death (17.1% vs 8.6%, p < 0.001) and myocardial infarction (9.5% vs 5.0%, p < 0.001) were, as expected, higher in patients with PAD compared to patients without PAD at 2 years. In conclusion, while PAD patients constitute a high-risk cohort with known higher adverse event rates, EECP led to similar short- and long-term improvements in angina and quality of life for individuals with PAD compared to those without PAD.

ST-elevation myocardial infarction: which patients do quality assurance programs include?

BACKGROUND: In the United States, efforts are underway to improve timely access to percutaneous coronary intervention in ST-elevation myocardial infarction (STEMI). The Joint Commission (TJC) and the American College of Cardiology National Cardiovascular Data Registry (NCDR) have developed standardized definitions and clinical performance measures for STEMI. The purpose of this study was to determine differences in 3 quality-assurance registries for STEMI patients. METHODS AND RESULTS: STEMI patients presenting to the Minneapolis Heart Institute at Abbott Northwestern Hospital (Minneapolis, Minn) are tracked by 3 distinct quality assurance programs: NCDR, TJC, and the level 1 MI registry (a regional system for percutaneous coronary intervention in STEMI which includes transfer patients). Over 1 year, we examined consecutive STEMI patients in level 1 and compared them with individuals meeting NCDR and TJC inclusion criteria. Of 501 STEMI patients treated using the level 1 MI protocol, 422 patients had a clear culprit (402 percutaneous coronary intervention, 13 coronary artery bypass grafting, 7 medical management). In the same period, 282 patients met inclusion criteria for NCDR (56% of the level 1 population), and 66 met inclusion criteria for TJC (13% of the level 1 population). Transfer patients (n=380) accounted for 87% of the discrepancy between level 1 and TJC. Pharmacoinvasive percutaneous coronary intervention (n=102) accounted for 47% of the discrepancy between level 1 and NCDR. CONCLUSIONS: Current inclusion criteria for enrollment in STEMI registries are not uniform. This may lead to variable quality assurance outcomes for the same patient cohort and has important implications for standardized quality measurement.

Enhanced external counterpulsation improves systolic blood pressure in patients with refractory angina.

BACKGROUND: Enhanced external counterpulsation (EECP) is a noninvasive treatment of patients with refractory angina. The immediate hemodynamic effects of EECP are similar to intra-aortic balloon pump counterpulsation, but EECP's effects on standard blood pressure measurements during and after treatment are unknown. METHODS: We evaluated systolic blood pressure (SBP) and diastolic blood pressure (DBP) for 108 consecutive patients undergoing EECP. Baseline SBP, DBP, and heart rate were compared for each patient before and after each EECP session, at the end of the course of EECP, and 6 weeks after the final EECP session. RESULTS: One hundred eight patients (mean age 66.4 +/- 11.2 years, 81% male) completed 36.5 +/- 5.1 EECP sessions per patient. Overall, based on 3,586 individual readings, EECP resulted in a decrease in mean SBP of 1.1 +/- 15.3 mm Hg at the end of each EECP session (P < .001), 6.4 +/- 18.2 mm Hg at the end the course of EECP (P < .001), and 3.7 +/- 17.8 mm Hg 6 weeks after the final EECP session (P = .07), with no significant change in DBP or heart rate. Stratifying by baseline SBP, a differential response was demonstrated: SBP increased in the 2 lowest strata (<100 mm Hg and 101-110 mm Hg) and decreased in the remaining strata (P < .001). Stratified differences were sustained after individual EECP sessions, at the end of the course of EECP, and 6 weeks after the final EECP session and were independent of changes in cardiovascular medications. CONCLUSIONS: Enhanced external counterpulsation improved SBP in patients with refractory angina. On average, EECP decreased SBP during treatment and follow-up; but for patients with low baseline SBP (<110 mm Hg), EECP increased SBP. The improvements in SBP may contribute to the clinical benefit of EECP.

Emerging therapies for refractory angina.

In recent years, improvements in both pharmacologic and revascularization therapies have greatly increased life expectancy for patients with coronary artery disease (CAD). As patients with more extensive CAD live longer, many develop myocardial ischemia and clinical angina that is not amenable to traditional revascularization therapy. Patients with severe, symptomatic, chronic CAD have been described as having refractory angina; they have also been termed "no-option" patients. This article discusses clinical management of this unique and growing group of patients and emerging therapeutic options including pharmacologic agents, enhanced external counterpulsation therapy, therapeutic angiogenesis, neurostimulation, and transmyocardial revascularization.

Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning.

CONTEXT: Carbon monoxide (CO) poisoning is a common cause of toxicological morbidity and mortality. Myocardial injury is a frequent consequence of moderate to severe CO poisoning. While the in-hospital mortality for these patients is low, the long-term outcome of myocardial injury in this setting is unknown. OBJECTIVE: To determine the association between myocardial injury and long-term mortality in patients following moderate to severe CO poisoning. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study of 230 consecutive adult patients treated for moderate to severe CO poisoning with hyperbaric oxygen and admitted to the Hennepin County Medical Center, a regional center for treatment of CO poisoning, between January 1, 1994, and January 1, 2002. Follow-up was through November 11, 2005. MAIN OUTCOME MEASURE: All-cause mortality. RESULTS: Myocardial injury (cardiac troponin I level > or =0.7 ng/mL or creatine kinase-MB level > or =5.0 ng/mL and/or diagnostic electrocardiogram changes) occurred in 85 (37%) of 230 patients. At a median follow-up of 7.6 years (range: in-hospital only to 11.8 years), there were 54 deaths (24%). Twelve of those deaths (5%) occurred in the hospital as a result of a combination of burn injury and anoxic brain injury (n = 8) or cardiac arrest and anoxic brain injury (n = 4). Among the 85 patients who sustained myocardial injury from CO poisoning, 32 (38%) eventually died compared with 22 (15%) of 145 patients who did not sustain myocardial injury (adjusted hazard ratio, 2.1; 95% confidence interval, 1.2-3.7; P = .009). CONCLUSION: Myocardial injury occurs frequently in patients hospitalized for moderate to severe CO poisoning and is a significant predictor of mortality.

Increased prevalence of coronary artery aneurysms among cocaine users.

BACKGROUND: Cocaine abuse has been implicated in multiple cardiovascular complications. Coronary artery aneurysms (CAAs) and ectasia occur in 0.2% to 5.3% of patients referred for angiography and are associated with atherosclerosis, Kawasaki's disease, and several rare disorders. After observing CAAs in multiple young cocaine users, we investigated the prevalence of CAAs among cocaine users undergoing coronary angiography. METHODS AND RESULTS: Clinical and angiographic characteristics of 112 consecutive patients with a history of cocaine use and coronary angiography were compared with a control group of similar age and risk factors from an existing angiographic database over the same time period. Coronary angiograms were independently read by 3 reviewers blinded to cocaine use. Cocaine users were young (mean age, 44 years), predominantly male (80%), and cigarette smokers (95%). Control patients had higher rates of diabetes (33%) and more severe coronary artery disease (P=0.01). Previous myocardial infarction was common in both groups (45% of cocaine users, 38% of control patients). Despite the frequent history of myocardial infarction among cocaine users, 48% had nonobstructive coronary artery disease. Among cocaine users, 34 of 112 (30.4%) had CAAs compared with 6 of 79 (7.6%) in the control group (P<0.001). Cocaine use was a strong predictor of CAA by univariate and multivariate analyses. CONCLUSIONS: This is the first description of an association between cocaine use and CAA. The prevalence of CAA among cocaine users was higher than expected (30.4%), given such a young cohort. Cocaine use may predispose to the formation of CAA, which may in turn be a contributing factor to myocardial infarction.

Cardiovascular manifestations of moderate to severe carbon monoxide poisoning.

OBJECTIVES: We describe the cardiovascular manifestations of carbon monoxide (CO) poisoning. BACKGROUND: Carbon monoxide poisoning is a common cause of toxicologic morbidity and mortality. Although the neurologic sequelae of CO poisoning have been well described, the cardiovascular consequences are limited to isolated case reports. METHODS: We reviewed the cardiovascular manifestations of 230 consecutive patients treated for moderate to severe CO poisoning in the hyperbaric oxygen chamber at Hennepin County Medical Center (HCMC), a regional center for treatment of CO poisoning. RESULTS: The mean age was 47.2 years with 72% men. Ischemic electrocardiogram (ECG) changes were present in 30% of patients, whereas only 16% had a normal ECG. Cardiac biomarkers (creatine kinase-MB fraction or troponin I) were elevated in 35% of patients. In-hospital mortality was 5%. CONCLUSIONS: Cardiovascular sequelae of CO poisoning are frequent, with myocardial injury assessed by biomarkers or ECG in 37% of patients. Patients admitted to the hospital with CO poisoning should have a baseline ECG and serial cardiac biomarkers.