Identification of vulnerable plaques and patients by intracoronary near-infrared spectroscopy and ultrasound (PROSPECT II): a prospective natural history study.

BACKGROUND: Near-infrared spectroscopy (NIRS) and intravascular ultrasound are promising imaging modalities to identify non-obstructive plaques likely to cause coronary-related events. We aimed to assess whether combined NIRS and intravascular ultrasound can identify high-risk plaques and patients that are at risk for future major adverse cardiac events (MACEs). METHODS: PROSPECT II is an investigator-sponsored, multicentre, prospective natural history study done at 14 university hospitals and two community hospitals in Denmark, Norway, and Sweden. We recruited patients of any age with recent (within past 4 weeks) myocardial infarction. After treatment of all flow-limiting coronary lesions, three-vessel imaging was done with a combined NIRS and intravascular ultrasound catheter. Untreated lesions (also known as non-culprit lesions) were identified by intravascular ultrasound and their lipid content was assessed by NIRS. The primary outcome was the covariate-adjusted rate of MACEs (the composite of cardiac death, myocardial infarction, unstable angina, or progressive angina) arising from untreated non-culprit lesions during follow-up. The relations between plaques with high lipid content, large plaque burden, and small lumen areas and patient-level and lesion-level events were determined. This trial is registered with ClinicalTrials.gov, NCT02171065. FINDINGS: Between June 10, 2014, and Dec 20, 2017, 3629 non-culprit lesions were characterised in 898 patients (153 [17%] women, 745 [83%] men; median age 63 [IQR 55-70] years). Median follow-up was 3·7 (IQR 3·0-4·4) years. Adverse events within 4 years occurred in 112 (13·2%, 95% CI 11·0-15·6) of 898 patients, with 66 (8·0%, 95% CI 6·2-10·0) arising from 78 untreated non-culprit lesions (mean baseline angiographic diameter stenosis 46·9% [SD 15·9]). Highly lipidic lesions (851 [24%] of 3500 lesions, present in 520 [59%] of 884 patients) were an independent predictor of patient-level non-culprit lesion-related MACEs (adjusted odds ratio 2·27, 95% CI 1·25-4·13) and non-culprit lesion-specific MACEs (7·83, 4·12-14·89). Large plaque burden (787 [22%] of 3629 lesions, present in 530 [59%] of 898 patients) was also an independent predictor of non-culprit lesion-related MACEs. Lesions with both large plaque burden by intravascular ultrasound and large lipid-rich cores by NIRS had a 4-year non-culprit lesion-related MACE rate of 7·0% (95% CI 4·0-10·0). Patients in whom one or more such lesions were identified had a 4-year non-culprit lesion-related MACE rate of 13·2% (95% CI 9·4-17·6). INTERPRETATION: Combined NIRS and intravascular ultrasound detects angiographically non-obstructive lesions with a high lipid content and large plaque burden that are at increased risk for future adverse cardiac outcomes. FUNDING: Abbott Vascular, Infraredx, and The Medicines Company.

Vulnerable plaques and patients: state-of-the-art.

Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term 'vulnerable plaque' was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of 'vulnerability' of a specific lesion to the more comprehensive goal of identifying patient 'cardiovascular vulnerability'. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and 'local' diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of 'high-risk' plaques occurring in 'vulnerable' patients.

Saphenous vein graft near-infrared spectroscopy imaging insights from the lipid core plaque association with clinical events near-infrared spectroscopy (ORACLE-NIRS) registry.

OBJECTIVES: We sought to examine near-infrared spectroscopy (NIRS) imaging findings of aortocoronary saphenous vein grafts (SVGs). BACKGROUND: SVGs are prone to develop atherosclerosis similar to native coronary arteries. They have received little study using NIRS. METHODS: We examined the clinical characteristics and imaging findings from 43 patients who underwent NIRS imaging of 45 SVGs at our institution between 2009 and 2016. RESULTS: The mean patient age was 67 ± 7 years and 98% were men, with high prevalence of diabetes mellitus (56%), hypertension (95%), and dyslipidemia (95%). Mean SVG age was 7 ± 7 years, mean SVG lipid core burden index (LCBI) was 53 ± 60 and mean maxLCBI4 mm was 194 ± 234. Twelve SVGs (27%) had lipid core plaques (2 yellow blocks on the block chemogram), with a higher prevalence in SVGs older than 5 years (46% vs. 5%, P = 0.002). Older SVG age was associated with higher LCBI (r = 0.480, P < 0.001) and higher maxLCBI4 mm (r = 0.567, P < 0.001). On univariate analysis, greater annual total cholesterol exposure was associated with higher SVG LCBI (r = 0.30, P = 0.042) and annual LDL-cholesterol and triglyceride exposure were associated with higher SVG maxLCBI4 mm (LDL-C: r = 0.41, P = 0.020; triglycerides: r = 0.36, P = 0.043). On multivariate analysis, the only independent predictor of SVG LCBI and maxLCBI4mm was SVG age. SVG percutaneous coronary intervention was performed in 63% of the patients. An embolic protection device was used in 96% of SVG PCIs. Periprocedural myocardial infarction occurred in one patient. CONCLUSIONS: Older SVG age and greater lipid exposure are associated with higher SVG lipid burden. © 2016 Wiley Periodicals, Inc.

Confirmation of the Intracoronary Near-Infrared Spectroscopy Threshold of Lipid-Rich Plaques That Underlie ST-Segment-Elevation Myocardial Infarction.

OBJECTIVE: In a previous exploratory analysis, intracoronary near-infrared spectroscopy (NIRS) found the majority of culprit lesions in ST-segment-elevation myocardial infarction (STEMI) to contain a maximum lipid core burden index in 4 mm (maxLCBI4mm) of >400. This initial study was limited by a small sample size, enrollment at a single center, and post hoc selection of the maxLCBI4mm ≥400 threshold. This study was designed a priori to substantiate the ability of NIRS to discriminate STEMI culprit from nonculprit segments and to confirm the performance of the maxLCBI4mm ≥400 threshold. APPROACH AND RESULTS: At 2 centers in the United States and Sweden, 75 STEMI patients underwent intracoronary NIRS imaging after establishing thrombolysis in myocardial infarction 3 flow, but before stenting. Blinded core laboratory analysis defined the culprit segment as the 10-mm segment distal to the proximal angiographic culprit margin. The remaining vessel was divided into contiguous 10-mm nonculprit segments. The maxLCBI4mm of culprit segments (median [interquartile range]: 543 [273-756]) was 4.4-fold greater than nonculprit segments (median [interquartile range]: 123 [0-307]; P<0.001). Receiver-operating characteristic analysis demonstrated that maxLCBI4mm differentiated culprit from nonculprit segments with high accuracy (c-statistic=0.83; P<0.001). A threshold maxLCBI4mm ≥400 identified STEMI culprit segments with a sensitivity of 64% and specificity of 85%. CONCLUSIONS: This study substantiates the ability of NIRS to accurately differentiate STEMI culprit from nonculprit segments and confirms that a threshold maxLCBI4mm ≥400 is detected by NIRS in the majority of STEMI culprits.

Near-Infrared Spectroscopy Enhances Intravascular Ultrasound Assessment of Vulnerable Coronary Plaque: A Combined Pathological and In Vivo Study.

OBJECTIVES: Pathological studies demonstrate the dual significance of plaque burden (PB) and lipid composition for mediating coronary plaque vulnerability. We evaluated relationships between intravascular ultrasound (IVUS)-derived PB and arterial remodeling with near-infrared spectroscopy (NIRS)-derived lipid content in ex vivo and in vivo human coronary arteries. APPROACH AND RESULTS: Ex vivo coronary NIRS and IVUS imaging was performed through blood in 116 coronary arteries of 51 autopsied hearts, followed by 2-mm block sectioning (n=2070) and histological grading according to modified American Heart Association criteria. Lesions were defined as the most heavily diseased 2-mm block per imaged artery on IVUS. IVUS-derived PB and NIRS-derived lipid core burden index (LCBI) of each block and lesion were analyzed. Block-level analysis demonstrated significant trends of increasing PB and LCBI across more complex atheroma (Ptrend <0.001 for both LCBI and PB). Lesion-based analyses demonstrated the highest LCBI and remodeling index within coronary fibroatheroma (Ptrend <0.001 and 0.02 versus all plaque groups, respectively). Prediction models demonstrated similar abilities of PB, LCBI, and remodeling index for discriminating fibroatheroma (c indices: 0.675, 0.712, and 0.672, respectively). A combined PB+LCBI analysis significantly improved fibroatheroma detection accuracy (c index 0.77, P=0.028 versus PB; net-reclassification index 43%, P=0.003), whereas further adding remodeling index did not (c index 0.80, P=0.27 versus PB+LCBI). In vivo comparisons of 43 age- and sex-matched patients (to the autopsy cohort) undergoing combined NIRS-IVUS coronary imaging yielded similar associations to those demonstrated ex vivo. CONCLUSIONS: Adding NIRS to conventional IVUS-derived PB imaging significantly improves the ability to detect more active, potentially vulnerable coronary atheroma.

Risk of myocardial infarction immediately after alcohol consumption.

BACKGROUND: Habitual moderate alcohol consumption is associated with a lower risk of acute myocardial infarction (MI), whereas heavy (binge) drinking is associated with higher cardiovascular risk. However, less is known about the immediate effects of alcohol consumption on the risk of acute MI and whether any association differs by beverage type or usual drinking patterns. METHODS: We conducted a case-crossover analysis of 3869 participants from the Determinants of Myocardial Infarction Onset Study who were interviewed during hospitalization for acute MI in one of the 64 medical centers across the United States in 1989-1996. We compared the observed number of times that each participant consumed wine, beer, or liquor in the hour preceding MI symptom onset with the expected frequency based on each participant's control information, defined as the number of times the participant consumed alcohol in the past year. RESULTS: Among 3869 participants, 2119 (55%) reported alcohol consumption in the past year, including 76 within 1 hour before acute MI onset. The incidence rate of acute MI onset was elevated 1.72-fold (95% confidence interval [CI] = 1.37-2.16) within 1 hour after alcohol consumption. The association was stronger for liquor than for beer or wine. The higher rate was not apparent for daily drinkers. For the 24 hours after consumption, there was a 14% lower rate (relative risk = 0.86 [95% CI = 0.79-0.95]) of MI compared with periods with no alcohol consumption. CONCLUSIONS: Alcohol consumption is associated with an acutely higher risk of MI in the subsequent hour among people who do not typically drink alcohol daily.

Risk of acute myocardial infarction after the death of a significant person in one's life: the Determinants of Myocardial Infarction Onset Study.

BACKGROUND: Acute psychological stress is associated with an abrupt increase in the risk of cardiovascular events. Intense grief in the days after the death of a significant person may trigger the onset of acute myocardial infarction (MI), but this relationship has not been systematically studied. METHODS AND RESULTS: We conducted a case-crossover analysis of 1985 participants from the multicenter Determinants of Myocardial Infarction Onset Study interviewed during index hospitalization for an acute MI between 1989 and 1994. We compared the observed number of deaths in the days preceding MI symptom onset with its expected frequency based on each patient's control information, defined as the occurrence of deaths in the period from 1 to 6 months before infarction. Among the 1985 subjects, 270 (13.6%) experienced the loss of a significant person in the prior 6 months, including 19 within 1 day of their MI. The incidence rate of acute MI onset was elevated 21.1-fold (95% confidence interval, 13.1-34.1) within 24 hours of the death of a significant person and declined steadily on each subsequent day. The absolute risk of MI within 1 week of the death of a significant person is 1 excess MI per 1394 exposed individuals at low (5%) 10-year MI risk and 1 per 320 among individuals at high (20%) 10-year risk. CONCLUSIONS: Grief over the death of a significant person was associated with an acutely increased risk of MI in the subsequent days. The impact may be greatest among individuals at high cardiovascular risk.

Frequency and location of yellow and disrupted coronary plaques in patients as detected by angioscopy.

BACKGROUND: Clarification of frequency and distribution of yellow plaques and disrupted plaques will increase understanding of acute coronary syndrome (ACS) onset. METHODS AND RESULTS: Consecutive patients with ACS (n=75) or without ACS (n=90) who received coronary angioscopic examination were studied. Distance from ostium to yellow plaques, diameter stenosis and vessel wall irregularity at the site of yellow plaques, their yellow color grade (grade 13) and if they had thrombus were analyzed. Yellow plaques with thrombus were regarded as disrupted. Average number of yellow plaques, grade-3 yellow plaques and disrupted yellow plaques per vessel was 4.0, 0.87 and 1.0, respectively. The number of grade-3 yellow plaques and disrupted yellow plaques per vessel were larger in ACS than in non-ACS patients. Yellow plaques were distributed diffusely in the right coronary artery but more in mid-segments in the left anterior descending coronary artery and left circumflex coronary artery. Diameter stenosis in the non-culprit segments was severer at disrupted than at non-disrupted yellow plaques. Vessel wall irregularity was detected more frequently at disrupted than at non-disrupted yellow plaques. CONCLUSIONS: Approximately 4 yellow plaques, 1 grade-3 yellow plaque and 1 disrupted yellow plaque were detected per vessel. About 25% of detected yellow plaques were disrupted. More grade-3 yellow plaques and disrupted yellow plaques were detected in ACS than in non-ACS patients. These findings strengthen the association between yellow plaques detected by angioscopy and ACS events.

Reducing Tobacco-Related Disability in Chronic Smokers.

Tobacco consumption (predominantly cigarettes) is the leading preventable cause of mortality worldwide. Although the major focus of strategies to reduce mortality from tobacco must include prevention of future generations from initially gaining access, some smokers are unwilling or unable to quit. Can the higher risk chronic smoker be identified and can their risk be reduced? The risk of adverse events in cigarette smokers is influenced by the intensity and duration of cigarette smoking or secondhand exposure, associated conventional risk factors, environmental stressors, and certain genetic variants and epigenetic modifiers. Recent data suggest that inflammatory markers such as high-sensitivity C-reactive protein (hs CRP) and targeted imaging can identify some smokers at higher risk. As smoking is prothrombotic, aspirin initiation and expanded statin use might reduce cardiovascular risk in those who do not presently meet criteria for these therapies, but further study is required. Thus, although advocacy for smoking cessation should always be the primary approach, increased efforts are needed to identify and potentially treat those who are unable or unwilling to quit.

2-Year Outcomes After Stenting of Lipid-Rich and Nonrich Coronary Plaques.

BACKGROUND: Autopsy studies suggest that implanting stents in lipid-rich plaque (LRP) may be associated with adverse outcomes. OBJECTIVES: The purpose of this study was to evaluate the association between LRP detected by near-infrared spectroscopy (NIRS) and clinical outcomes in patients with coronary artery disease treated with contemporary drug-eluting stents. METHODS: In this prospective, multicenter registry, NIRS was performed in patients undergoing coronary angiography and possible percutaneous coronary intervention (PCI). Lipid core burden index (LCBI) was calculated as the fraction of pixels with the probability of LRP >0.6 within a region of interest. MaxLCBI4mm was defined as the maximum LCBI within any 4-mm-long segment. Major adverse cardiac events (MACE) included cardiac death, myocardial infarction, definite or probable stent thrombosis, or unplanned revascularization or rehospitalization for progressive angina or unstable angina. Events were subcategorized as culprit (treated) lesion-related, nonculprit (untreated) lesion-related, or indeterminate. RESULTS: Among 1,999 patients who were enrolled in the COLOR (Chemometric Observations of Lipid Core Plaques of Interest in Native Coronary Arteries Registry), PCI was performed in 1,621 patients and MACE occurred in 18.0% of patients, of which 8.3% were culprit lesion-related, 10.7% were nonculprit lesion-related, and 3.1% were indeterminate during 2-year follow-up. Complications from NIRS imaging occurred in 9 patients (0.45%), which resulted in 1 peri-procedural myocardial infarction and 1 emergent coronary bypass. Pre-PCI NIRS imaging was obtained in 1,189 patients, and the 2-year rate of culprit lesion-related MACE was not significantly associated with maxLCBI4mm (hazard ratio of maxLCBI4mm per 100: 1.06; 95% confidence interval: 0.96 to 1.17; p = 0.28) after adjusting clinical and procedural factors. CONCLUSIONS: Following PCI with contemporary drug-eluting stents, stent implantation in NIRS-defined LRPs was not associated with increased periprocedural or late adverse outcomes compared with those without significant lipid.

Contemporary rationale for non-invasive imaging of adverse coronary plaque features to identify the vulnerable patient: a Position Paper from the European Society of Cardiology Working Group on Atherosclerosis and Vascular Biology and the European Association of Cardiovascular Imaging.

Atherosclerotic plaques prone to rupture may cause acute myocardial infarction (MI) but can also heal without causing an event. Certain common histopathological features, including inflammation, a thin fibrous cap, positive remodelling, a large necrotic core, microcalcification, and plaque haemorrhage are commonly found in plaques causing an acute event. Recent advances in imaging techniques have made it possible to detect not only luminal stenosis and overall coronary atherosclerosis burden but also to identify such adverse plaque characteristics. However, the predictive value of identifying individual adverse atherosclerotic plaques for future events has remained poor. In this Position Paper, the relationship between vulnerable plaque imaging and MI is addressed, mainly for non-invasive assessments but also for invasive imaging of adverse plaques in patients undergoing invasive coronary angiography. Dynamic changes in atherosclerotic plaque development and composition may indicate that an adverse plaque phenotype should be considered at the patient level rather than for individual plaques. Imaging of adverse plaque burden throughout the coronary vascular tree, in combination with biomarkers and biomechanical parameters, therefore holds promise for identifying subjects at increased risk of MI and for guiding medical and invasive treatment.

An exploratory prospective study of marijuana use and mortality following acute myocardial infarction.

BACKGROUND: The relationship of marijuana use with coronary heart disease, including prognosis among patients with coronary heart disease, is uncertain. METHODS: We conducted an inception cohort study of 1913 adults hospitalized with myocardial infarction at 45 US hospitals between 1989 and 1994, with a median follow-up of 3.8 years. We ascertained total mortality according to self-reported marijuana use in the preceding year. RESULTS: A total of 52 patients reported marijuana use during the prior year, and 317 patients died during follow-up. Compared with nonuse, marijuana use less than weekly was associated with a hazard ratio of 2.5 (95% CI, 0.9-7.3). The corresponding hazard ratio for weekly use or more was 4.2 (95% CI, 1.2-14.3). The age- and sex-adjusted hazard ratios associated with any use were 1.9 (95% CI, 0.6-6.3) for cardiovascular mortality and 4.9 (95% CI, 1.6-14.7) for noncardiovascular mortality. In a comparison of 42 marijuana users and 42 other patients matched on propensity scores, there were 6 deaths among marijuana users and one among non-users (log-rank P = .06). CONCLUSIONS: These preliminary results suggest possible hazards of marijuana for patients who survive acute myocardial infarction. Although marijuana use has not been associated with mortality in other populations, it may pose particular risk for susceptible individuals with coronary heart disease.

Anxiety and anger immediately prior to myocardial infarction and long-term mortality: Characteristics of high-risk patients.

OBJECTIVE: Acute high levels of anger and anxiety are associated with an elevated risk of myocardial infarction (MI) in the following two hours. MIs preceded by these acute negative emotions may also have a poor long-term prognosis, but information about high-risk patients is lacking. We examined whether young age and female sex are associated with MIs that are preceded by negative emotions and whether age and sex moderate the subsequent increased mortality risk following MI preceded by negative emotions. METHODS: We conducted a secondary analysis of the Determinants of Myocardial Infarction Onset Study (N=2176, mean age=60.1±12.3years, 29.2% women). Anxiety and anger immediately prior to (0-2h) MI and the day before (24-26h) MI were assessed using a structured interview. Subsequent 10-year all-cause mortality was determined using the US National Death Index. RESULTS: Anxiety during the 0-2h pre-MI period was associated with younger age (OR=0.98,95% CI=0.96-0.99 per year) and female sex (OR=1.50,95% CI=1.11-2.02). Anger in the 0-2h pre-MI period was also associated with younger age (OR=0.95,95% CI=0.94-0.96) but not with sex (OR=0.93,95% CI=0.67-1.28). During follow-up, 580 (26.7%) patients died. Mortality rate was higher if MI occurred immediately after high anxiety, particularly in patients ≥65years (HR=1.80,95% CI=1.28-2.54) vs. younger patients (HR=0.87,95% CI=0.55-1.40; p-interaction=0.015). Other interactions with sex or anger were not significant. CONCLUSIONS: Patients with high anxiety or anger levels in the critical 2-hour period prior to MI are younger than those without such emotional precipitants. In addition, pre-MI anxiety is associated with an elevated 10-year mortality risk in patients aged ≥65years.

Multimodality Intracoronary Imaging With Near-Infrared Spectroscopy and Intravascular Ultrasound in Asymptomatic Individuals With High Calcium Scores.

BACKGROUND: This study sought to determine the frequency of large lipid-rich plaques (LRP) in the coronary arteries of individuals with high coronary artery calcium scores (CACS) and to determine whether the CACS correlates with coronary lipid burden. METHODS AND RESULTS: Combined near-infrared spectroscopy and intravascular ultrasound was performed in 57 vessels in 20 asymptomatic individuals (90% on statins) with no prior history of coronary artery disease who had a screening CACS ≥300 Agatston units. Among 268 10-mm coronary segments, near-infrared spectroscopy images were analyzed for LRP, defined as a bright yellow block on the near-infrared spectroscopy block chemogram. Lipid burden was assessed as the lipid core burden index (LCBI), and large LRP were defined as a maximum LCBI in 4 mm ≥400. Vessel plaque volume was measured by quantitative intravascular ultrasound. Vessel-level CACS significantly correlated with plaque volume by intravascular ultrasound (r=0.69; P<0.0001) but not with LCBI by near-infrared spectroscopy (r=0.24; P=0.07). Despite a high CACS, no LRP was detected in 8 (40.0%) subjects. Large LRP having a maximum LCBI in 4 mm ≥400 were infrequent, found in only 5 (25.0%) of 20 subjects and in only 5 (1.9%) of 268 10-mm coronary segments analyzed. CONCLUSIONS: Among individuals with a CACS ≥300 Agatston units mostly on statins, CACS correlated with total plaque volume but not LCBI. This observation may have implications on coronary risk among individuals with a high CACS considering that it is coronary LRP, rather than calcification, that underlies the majority of acute coronary events.

Intravascular ultrasound and near-infrared spectroscopic features of coronary lesions with intraplaque haemorrhage.

AIMS: Intraplaque haemorrhage is considered a major contributor to lesion progression. We assessed coronary lesions with intraplaque haemorrhage using intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS). METHODS AND RESULTS: We evaluated coronary arteries from autopsy hearts using 40MHz IVUS and NIRS and compared the imaging findings to histopathology. A total of 2324 2-mm long histological segments from 101 coronary arteries from 56 autopsy hearts were included. Intraplaque haemorrhage was found pathologically in 0.8% (18/2324) of segments. Segments with intraplaque haemorrhage had more fibroatheromas (FAs) with a greater IVUS plaque burden, a greater prevalence of IVUS echolucent zones, and a higher NIRS-lipid core burden index (LCBI) compared to segments without intraplaque haemorrhage (FAs: 72.2% vs. 18.3%, P < 0.0001; plaque burden: 59.7% [95% confidence interval: 55.5, 64.0] vs. 48.6% [45.8, 51.3], P < 0.0001; echolucent zones: 88.9% vs. 2.8%, P < 0.0001; NIRS-LCBI: 176 [88, 264] vs. 72 [53, 91], P = 0.02). The 16 IVUS superficial echolucent zones with intraplaque haemorrhage had more late FAs but shorter echolucent zone lengths (0.9 mm [0.7, 1.1] vs. 1.7 mm [1.5, 1.9], P < 0.0001) compared to 65 IVUS superficial echolucent zones without intraplaque haemorrhage. CONCLUSIONS: Intracoronary imaging features consistent with intraplaque haemorrhage included a greater plaque burden, a higher NIRS-LCBI, and a greater prevalence of IVUS echolucent zones compared to lesions without intraplaque haemorrhage.

Binge drinking and mortality after acute myocardial infarction.

BACKGROUND: Moderate drinkers have a lower risk of mortality after myocardial infarction (MI). Although binge drinking has been associated with a higher risk of MI in some studies, its relation to prognosis after MI is uncertain. METHODS AND RESULTS: In a prospective, inception cohort study conducted at 45 US hospitals, 1935 patients hospitalized with a confirmed MI between 1989 and 1994 underwent detailed personal interviews. Patients reported their usual frequency of binge drinking of beer, wine, and liquor, defined as intake of 3 or more drinks within 1 to 2 hours, and were followed up for mortality for a median of 3.8 years. Of 1919 eligible patients, 250 (94% men) reported binge drinking during the prior year, and a total of 318 patients died during follow-up. Binge drinkers had a 2-fold higher risk of mortality than drinkers who did not binge (hazard ratio, 2.0; 95% confidence interval, 1.3 to 3.0). A comparison of 192 binge drinkers and 192 other patients matched on propensity scores yielded a similar result. The association between binge drinking and total mortality tended to be similar among patients whose usual alcohol intake was light or heavier and for binge drinkers who consumed beer, wine, or liquor. Usual alcohol intake was inversely associated with mortality, but binge drinking completely attenuated this relation. CONCLUSIONS: Our results suggest that alcohol consumption may be linked to potential hazards among patients who survive acute MI. Although moderate intake has been associated with lower mortality, binge drinking, even among light drinkers, appears to be associated with 2-fold higher mortality.

Depression as a predictor for appropriate shocks among patients with implantable cardioverter-defibrillators: results from the Triggers of Ventricular Arrhythmias (TOVA) study.

OBJECTIVES: We sought to examine the relationship between symptoms of depression and shock-treated ventricular arrhythmias among implantable cardioverter-defibrillator (ICD) patients. BACKGROUND: Depression predicts mortality in patients with coronary artery disease (CAD), but whether this is via an increased risk of fatal ventricular arrhythmias is unclear. METHODS: We prospectively analyzed data on symptoms of depression and risk of ventricular arrhythmia (ventricular tachycardia/ventricular fibrillation [VT/VF]) resulting in ICD discharge in the Triggers of Ventricular Arrhythmias (TOVA) study. Symptoms were assessed by the Center for Epidemiologic Studies-Depression (CES-D) scale. Scores of 16 to 26 and > or =27 represented mild and moderate/severe depression, respectively. The Cox and Anderson-Gill proportional hazards models were used to test for associations among all patients and patients with CAD. RESULTS: Among 645 patients with baseline assessments, 90 (14%) were mildly depressed and 25 (3.9%) were moderately to severely depressed. Moderate/severe depression was associated with time to first shock for VT/VF (hazard ratio [HR] 3.2, 95% confidence interval [CI] 1.1 to 9.9) and all shocks for VT/VF including recurrent episodes (HR 3.2, 95% CI 1.2 to 8.6). Among the 476 CAD patients, the association with time to first shock (HR 6.4, 95% CI 1.9 to 21.1) and all shocks (HR 8.3, 95% CI 2.9 to 23.3) remained. The risk of shock for VT/VF was associated with depression severity in the total population (p for trend = 0.02) and among patients with CAD (p < 0.01), even after controlling for multiple confounders. CONCLUSIONS: More severe symptoms of depression predict shocks for VT/VF among ICD patients. The elevated risk of VT/VF among patients with CAD and depression suggests that arrhythmia may contribute significantly to total mortality in this subgroup.