Antithrombotic regimens in patients with indication for long-term anticoagulation undergoing coronary interventions-systematic analysis, review of literature, and implications on management.

There is lack of consensus regarding use of antithrombotic therapy (AT) in patients with indications for long-term anticoagulation who undergo percutaneous coronary intervention. We sought to evaluate the safety and efficacy of various antithrombotic regimens in this patient population. We conducted a Medline search for all English language, full-text articles from January 2000 to June 2009 that evaluated major cardiovascular outcomes in patients with indications for anticoagulation who undergo percutaneous coronary intervention. Data were analyzed from these studies to calculate annual incidence of major bleeding, stroke, and stent thrombosis with various antithrombotic regimens. Major bleeding events were calculated at 30 days and at 1 year. Ten retrospective studies, 1 post hoc analysis of a major registry, and 2 prospective studies qualified for our analysis. Atrial fibrillation was the most common indication for anticoagulation. Risk of major bleeding was 1.5% at 30 days and 5.2% at 1 year with triple AT (aspirin + warfarin + clopidogrel/ticlopidine). Dual antiplatelet therapy (aspirin + clopidogrel/ticlopidine) was associated with 2.4% annual risk of major bleeding. The annual incidence of both ischemic stroke and stent thrombosis was 1% with triple antithrombotic regimen. Risk of major bleeding increases proportionately with incremental duration of triple AT. Triple AT is effective in the prevention of ischemic stroke and stent thrombosis. Dual antiplatelet regimen is effective in patients with low annual risk of ischemic stroke (<4%; CHADS-2 score <2) due to lower annual risk of bleeding associated with this regimen (2.4%).

Effect of carvedilol versus metoprolol CR/XL on mortality in patients with heart failure treated with cardiac resynchronization therapy: a COX multivariate regression analysis.

We investigated in 136 consecutive patients with heart failure receiving cardiac resynchronization therapy (CRT) the effect of carvedilol versus metoprolol CR/XL versus no beta blocker on mortality. Of the 136 patients, 42 (31%) were on carvedilol, 80 (59%) were on metoprolol CR/XL, and 14 (10%) were not on a beta blocker. A decrease of left ventricular end-systolic volume ≥15% after CRT was defined as a positive response to CRT. Of the 136 patients, 62 (46%) responded to CRT. It was found that both carvedilol and metoprolol CR/XL were not related to CRT response on using Cox univariate regression analysis. Twenty-two of the 136 patients (16%) died during follow-up of 17 ± 10 months after initiating CRT. Mortality occurred in 14 of 80 patients (18%) on metoprolol CR/XL, in 3 of 42 patients (7%) on carvedilol, and in 5 of 14 patients (36%) not on beta blockers (P = 0.04). After adjustment for age, gender, and the variables with significant differences by Cox univariate regression, both carvedilol (hazard ratio = 0.14; P = 0.03; 95% confidence interval = 0.02-0.86) and metoprolol CR/XL (hazard ratio = 0.19; P = 0.02; 95% confidence interval = 0.04-0.80) were found to be related to mortality by Cox multivariate regression.

A patient selection score for cardiac resynchronization therapy.

BACKGROUND: We hypothesized a patient selection score (PSS) may improve patient selection for cardiac resynchronization therapy (CRT). METHODS: Of 136 patients who received CRT, group A included 100 study patients and group B 36 patients for validation. A positive response to CRT was a left ventricular (LV) end-systolic volume decrease of ≥15% and survival from heart failure at end of follow-up. RESULTS: Of 100 group A patients, 37 (37%) were CRT responders during 14-month follow-up. A 7-point PSS was generated based on six variables. The cutoff point for PSS to predict a positive response to CRT was >4 by receiver operating characteristic (ROC) analysis. The area under the ROC curve (AUC) for PSS to predict CRT response was 0.94 (P = 0.0001). CRT responders in patients with a PSS > 4 and ≤4 were 33/40 (83%), and 4/60 (7%), respectively (P < 0.001). Multivariate Cox proportional regression analysis showed that PSS was related to CRT response (hazard ratio = 10.3, P < 0.0001). The CRT response rate in patients with a PSS > 4 in Group B was also significantly higher compared to a PSS ≤ 4 (88% vs. 16%, P < 0.001). The AUC for PSS to predict a CRT response in Group B was 0.91 (P = 0.0001). CONCLUSIONS: Patients with a PSS >4 are the most likely to respond to CRT. Using this score system, a PSS score >4 can predict the probability of a CRT response up to 88% in patients with heart failure and a wide QRS duration.

Effect of medical therapy on left ventricular ejection fraction in patients with systolic heart failure and narrow QRS duration with and without ischemic heart disease and left ventricular mechanical dyssynchrony.

We studied 99 consecutive patients with class III-IV systolic heart failure with a left ventricular ejection fraction (LVEF) < or =35% and a QRS duration <120 milliseconds. Patients with cardiac resynchronization therapy were excluded. Echocardiography was performed in all patients before and after optimal standard heart failure therapy. The septal-to-posterior wall motion delay (SPWMD) > or =130 milliseconds on echocardiogram was defined as left ventricular mechanical dyssynchrony (LVMD). Sixty-nine of 99 patients (70%) had ischemic heart disease. During follow-up of 15.2 +/- 9.8 months, LVEF improvement > or =15% was greater patients in nonischemic group (50%, 15/30) than in ischemic group (9%, 6/69; P < 0.001). After adjustment for age, gender, and clinical and echocardiographic characteristics, ischemic heart disease and grade of coronary disease were persistently related to LVEF improvement > or =15% (P = 0.03 and 0.02, respectively). Twenty of 99 patients (20%) had SPWMD > or =130 milliseconds (LVMD group), and 79 of 99 patients (80%) had SPWMD <130 milliseconds (non-LVMD group). LVEF increased in both groups (P = 0.005) during follow-up, but the percentage of patients with LVEF improvement > or =15% in LVMD was greater compared with patients without LVMD (40% versus 16%, respectively, P = 0.03). In conclusion, the improvement of LVEF in patients with systolic heart failure and narrow QRS was greater in patients with nonischemic heart disease and LVMD compared with patients with ischemic heart disease and absence of LVMD during medical therapy without cardiac resynchronization therapy.

Cardiac resynchronization therapy in patients with intrinsic and right ventricular pacing-induced left bundle branch block pattern.

We studied 95 consecutive patients, mean age 70 years, who received cardiac resynchronization therapy (CRT) for class III or IV heart failure with a left ventricular (LV) ejection fraction < or =35% and a QRS duration > or =120 ms. Sixty-seven patients had intrinsic left bundle branch block (LBBB) (group 1), and 28 patients had right ventricular pacing-induced LBBB (group 2). The time difference (TPW-TDI) between onset of QRS to the end of LV ejection by pulsed wave Doppler and onset of QRS to the end of systolic wave in the basal segment with greatest delay by tissue Doppler imaging was measured before CRT and at the last follow-up after CRT. TPW-TDI >50 ms was defined as left ventricular mechanical dyssynchrony. A positive response to CRT was defined as LV volume at end-systole decreasing > or =15% after CRT. The percentage of CRT responders in group 2 was significantly greater than that in group 1 (68% versus 42%, P = 0.04) during follow-up of 16 months. After adjusting for age, gender, and clinical features, this pattern of CRT response persisted (P = 0.008). Similarly, there was a greater reduction in QRS duration in group 2 (178 ms) after CRT versus 154 ms for group 1, P = 0.01. There was no significant difference in TPW-TDI between the 2 groups at baseline or at follow-up. There was no significant difference in mortality (15% versus 14%) and Kaplan-Meier survival plot during follow-up. Patients with heart failure and right ventricular pacing-induced LBBB have a better response rate to CRT than patients with intrinsic LBBB. The change in left ventricular mechanical dyssynchrony after CRT was similar in these 2 groups of patients.

Thromboembolism in patients with atrial fibrillation with and without left atrial thrombus documented by transesophageal echocardiography.

The incidence of cerebrovascular events (CVEs) was investigated in 95 consecutive patients with atrial fibrillation (AF) with left atrial thrombus (LAT) diagnosed by transesophageal echocardiography (TEE) and in 131 age- and sex-matched AF patients without LAT. Compared with patients without LAT, patients with LAT had a larger left atrial diameter (49 versus 44 mm, P < 0.0001), a lower left ventricular ejection fraction (40% versus 50%, P < 0.0001), a higher prevalence of spontaneous echocardiographic contrast (88% versus 25%, P < 0.001), a reduced left atrial appendage emptying velocity (0.25 versus 0.41 cm/s, P < 0.0001), and less use of antiarrhythmic drugs (61% versus 76%, P = 0.03). Before TEE, the prevalence of prior CVE was higher in LAT patients (20%) compared with patients without LAT (8%) (P = 0.01). Fifty-four of 95 LAT patients (57%) and 81 of 131 non-LAT patients (62%) were on warfarin before TEE. The incidence of prior CVE in LAT patients without warfarin (32%) was higher than that in non-LAT patients without warfarin (10%) (P = 0.02). The mortality rate in LAT patients with an international normalized ratio (INR) >or= 2.0 (42%) was higher than that in patients without LAT and an INR >or= 2.0 (11%) (P < 0.001). Fifty-one of 95 LAT patients (54%) underwent repeat TEE before cardioversion (48 patients received warfarin therapy). The thrombus resolved in 40 of 51 patients (78%) after the first TEE. There was no significant difference in INR between the patients with persistent and resolved LAT. AF patients with persistent LAT had a higher incidence of CVE (45%) than the patients with resolved LAT (5%) (P = 0.003). We suggest that patients with LAT be treated with warfarin to maintain an INR between 2.5 and 3.5 rather than between 2.0 and 3.0 because they are at a high risk for new thromboembolism.

Are the extent, location, and score of segmental wall motion abnormalities related to cardiac resynchronization therapy response?

BACKGROUND: We hypothesized that segmental wall motion abnormalities (WMAs) are related to cardiac resynchronization therapy (CRT) response. METHODS: We studied 108 patients who received CRT, 69 with ischemic and 39 with nonischemic heart disease. A wall motion score index (WMSI) was analyzed using a 17-segment model and calculated by the total score/number of segments analyzed. A decrease of left ventricular end systolic volume > or =15% after CRT was defined as a positive response to CRT. RESULTS: Of 108 patients, 1,054/1,836 segments (57%) had WMAs. The mean WMSI was 2.06 in patients with ischemic heart disease and 1.04 in patients with nonischemic heart disease (P < 0.0001). The area under the receiver operating characteristic curve for a WMSI predicting a positive response to CRT was 0.70 (P = 0.0001). The cutoff point was a WMSI < or =2 for prediction of a positive response to CRT. After adjustment for age, gender, and clinical features, the WMSI persistently related to CRT responders (P = 0.01). During 15-month follow-up, the percentage of CRT nonresponders in patients with a WMSI >2 was significantly higher (82%) compared to patients with a WMSI < or =2 (47%, P = 0.005) and nonischemic heart disease (36%, P < 0.001). In 59 patients with left ventricular mechanical dyssynchrony, the percentage of negative responders to CRT in patients with a WMSI >2, < or =2, and nonischemic heart disease were 53% (8 of 15), 16% (3 of 19) and 0% (0 of 25), respectively (P < 0.001). CONCLUSIONS: A large extent of WMAs and a WMSI >2 predicted a poorer CRT response.

Treatment of refractory angina pectoris.

Refractory angina pectoris is defined as Canadian Cardiovascular Society class III or IV angina, where there is marked limitation of ordinary physical activity or inability to perform ordinary physical activity without discomfort, with an objective evidence of myocardial ischemia and persistence of symptoms despite optimal medical therapy, life style modification treatments, and revascularization therapies. The patients with refractory angina pectoris may have diffuse coronary artery disease, multiple distal coronary stenoses, and or small coronary arteries. In addition, a substantial portion of these patients cannot achieve complete revascularization and continue to experience residual anginal symptoms that may impair quality of their life and increase morbidity. This represents an end-stage coronary artery disease characterized by a severe myocardial insufficiency usually with impaired left ventricular function. As the life expectancy is increasing, patients with angina pectoris refractory to conventional antianginal therapeutics are a challenging problem. We review the nonconventional therapies to treat the refractory angina pectoris, including pharmacotherapy, therapeutic angiogenesis, transcutaneus electrical nerve and spinal cord stimulation, enhanced external counterpulsation, surgical transmyocardial laser revascularization, percutaneous transmyocardial laser revascularization, percutaneous in situ coronary venous arterializations, and percutaneous in situ coronary artery bypass. These therapies are not supported by a large body of data and have only a complementary role; therefore, the aggressive traditional and proven treatment of angina pectoris should be continued along with these therapies, used on an individual basis.

Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis.

Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.

Pseudo-pseudoaneurysm of the left ventricle: a rare complication of acute myocardial infarction--a case report and literature review.

Rupture of the cardiac wall is usually a fatal complication of acute myocardial infarction within the first 2 weeks. However, in certain cases a ruptured ventricular wall is contained by overlying adherent pericardium called pseudoaneurysm, whereas a true aneurysm is one that is caused by scar formation resulting in thinning of the myocardium. The patients with pseudoaneurysm may survive until the aneurysm ruptures. In exceedingly rare instance, the rupture of the myocardium is not transmural but remains circumscribed within the ventricular wall itself, but in communication with the ventricular cavity. This finding is defined as pseudo-pseudoaneurysm. The authors report a case of postinfarction posterobasal pseudo-pseudoaneurysm along with review of the literature on the subject.

Cardiac papillary fibroelastoma: a comprehensive analysis of 725 cases.

BACKGROUND: With the advent of echocardiography, cardiac papillary fibroelastoma (CPF) is being increasingly reported. The demographics, clinical characteristics, pathological features, treatment, and prognosis of CPF are examined. DATA COLLECTIONS: Cases, case series and related articles on the subject in all languages were identified through a comprehensive literature search. RESULTS AND CONCLUSIONS: Seven hundred twenty-five cases of CPF were identified. Males comprised 55% of patients. Highest prevalence was in the 8th decade of life. The valvular surface was the predominant locations of tumor. The most commonly involved valve was the aortic valve, followed by the mitral valve. The left ventricle was the predominant nonvalvular site involved. No clear risk factor for development of CPF has been reported. Size of the tumor varied from 2 mm to 70 mm. Clinically, CPFs have presented with transient ischemic attack, stroke, myocardial infarction, sudden death, heart failure, presyncope, syncope, pulmonary embolism, blindness, and peripheral embolism. Tumor mobility was the only independent predictor of CPF-related death or nonfatal embolization. Symptomatic patients should be treated surgically because the successful complete resection of CPF is curative and the long-term postoperative prognosis is excellent. The symptomatic patients who are not surgical candidates could be offered long-term oral anticoagulation, although no randomized controlled data are available on its efficacy. Asymptomatic patients could be treated surgically if the tumor is mobile, as the tumor mobility is the independent predictor of death or nonfatal embolization. Asymptomatic patients with nonmobile CPF could be followed-up closely with periodic clinical evaluation and echocardiography, and receive surgical intervention when symptoms develop or the tumor becomes mobile.

Effect of spironolactone on endothelial function in patients with congestive heart failure on conventional medical therapy.

We prospectively studied the effect of spironolactone, an aldosterone antagonist, on endothelial function in patients with advanced congestive heart failure (CHF) using the brachial artery reactivity method. Twenty patients optimized on conventional CHF therapy were treated with spironolactone, and brachial artery flow- mediated dilation was measured at baseline and at 4 and 8 weeks. Spironolactone improved endothelial function at 4 weeks, and sustained the improvement at 8 weeks, in patients with CHF on conventional medical therapy, presumably due to reversal of aldosterone impairment of endothelial nitric oxide activity.

Clinical, diagnostic, and management perspectives of aortic dissection.

The incidence of aortic dissection ranges from 5 to 30 cases per million people per year, depending on the prevalence of risk factors in the study population. Although the disease is uncommon, its outcome is frequently fatal, and many patients with aortic dissection die before presentation to the hospital or prior to diagnosis. While pain is the most common symptom of aortic dissection, more than one-third of patients may develop a myriad of symptoms secondary to the involvement of the organ systems. Physical findings may be absent or, if present, could be suggestive of a diverse range of other conditions. Keeping a high clinical index of suspicion is mandatory for the accurate and rapid diagnosis of aortic dissection. CT scanning, MRI, and transesophageal echocardiography are all fairly accurate modalities that are used to diagnose aortic dissection, but each is fraught with certain limitations. The choice of the diagnostic modality depends, to a great extent, on the availability and expertise at the given institution. The management of aortic dissection has consisted of aggressive antihypertensive treatment, when associated with systemic hypertension, and surgery. Recently, endovascular stent placement has been used for the treatment of aortic dissection in select patient populations, but the experience is limited. The technique could be an option for patients who are poor surgical candidates, or in whom the risk of complications is gravely high, especially so in the patients with distal dissections. The clinical, diagnostic, and management perspectives on aortic dissection and its variants, aortic intramural hematoma and atherosclerotic aortic ulcer, are reviewed.

Acute ventricular rate control in atrial fibrillation and atrial flutter.

Atrioventricular node blocking agents including beta-adrenergic blockers, non-dihydropyridine calcium channel blockers and digoxin are usually effective in controlling ventricular rate in atrial fibrillation and flutter. Intravenous beta-blockers and non-dihydropyridine calcium channel blockers are equally effective in rapidly controlling the ventricular rate. The addition of digoxin to the regimen causes a favorable outcome but digoxin as a single agent is generally less effective in slowing the ventricular rate in acute setting. Clonidine, magnesium, and amiodarone have also been used for acute ventricular rate control in atrial fibrillation. Limited data suggest that combination regimens provide better ventricular rate control than any agent alone. The agent of first choice is usually individualized depending upon the clinical situation. Beta-blockers are preferable in patients with myocardial ischemia, myocardial infarction and hyperthyroidism and in post-operative state, but should be avoided in patients with bronchial asthma and chronic obstructive pulmonary disease where non-dihydropyridine calcium channel blockers are preferred. Beta-blockers are preferred drugs used for acute ventricular rate control in atrial fibrillation during pregnancy. In atrial fibrillation with Wolff-Parkinson-White syndrome, beta-blockers, calcium channel blockers and digoxin should be avoided, as these drugs are selective atrioventricular node blockers without slowing conduction through the accessory pathway, which can lead to increased transmission of impulses preferentially through the accessory pathway and precipitate ventricular fibrillation. The drug of choice for atrial fibrillation in pre-excitation syndrome is procainamide but propafenone, flecainide and disopyramide have also been used. When clinical condition is unstable or patient is hemodynamically compromised, immediate electrical cardioversion is the treatment of choice, as the best measure to control ventricular rate is by conversion to sinus rhythm. Factors precipitating rapid ventricular rate should be treated as well.

Gender significance of ST-segment deviation detected by ambulatory (Holter) monitoring.

OBJECTIVE: To evaluate the gender influence in diagnostic and prognostic value of Holter-detected ST-segment deviation. METHODS: Two-hundred seventy-seven consecutive patients (196 men) who underwent coronary angiography for evaluation of chest pain were studied with 24-h Holter monitoring within 72 h of coronary angiography, and were followed up for 65+/-21 months. RESULTS: Men had a higher prevalence of coronary artery disease (169 of 196, 86%) compared to that of women (54 of 81, 67%), p<0.00025. Thirty-three (17%) men and 15 (19%) women had ST-segment deviation during 24-h recording. The sensitivity, specificity and positive predictive values of ST-segment deviation (elevation, depression, or both) for the detection of significant coronary artery disease were similar in men and women. The negative predictive values were significantly higher in women than men for ST-segment deviation (36% vs. 15%, p<0.001), ST-segment elevation (35% vs. 14%, p<0.001), and ST-segment depression (34% vs. 15%, p<0.001). Similarly, the diagnostic accuracies were significantly higher in women than men for ST-segment deviation (44% vs. 29%, p<0.025), ST-segment elevation (38% vs. 19%, p<0.001), and ST-segment depression (40% vs. 24%, p<0.025). There was no significant difference in composite end-point of events (mortality, nonfatal myocardial infarction, unstable angina, and coronary revascularization) in men versus women with ST-segment deviation (elevation, depression, or both). CONCLUSION: Holter-detected ST-segment deviation has a higher negative predictive value and diagnostic accuracy for detection of significant coronary artery disease in women than in men, although the prognostic values are not significantly different between men and women.

Improving the cardio protective effect of aFGF in ischemic myocardium with ultrasound-mediated cavitation of heparin modified microbubbles: preliminary experiment.

Ultrasound (US)-mediated cavitation of microbubbles has evolved into a new tool for organ-specific gene and drug delivery. This paper was to investigate the feasibility of acidic fibroblast growth factor (aFGF) intravenous delivery to the ischemic myocardium of rats by ultrasonic microbubbles modified with heparin. Heparin modified microbubbles (HMB) were prepared by the freeze-dried method. Acute myocardial infarction (AMI) model was established and the cardio protective effect of the aFGF combing with HMB (aFGF-HMB) under US-mediated cavitation technique was investigated. aFGF-HMB combined with US-mediated cavitation technique was examined by ECG. Ejection fraction (EF), fractional shortening (FS) and left ventricular diastolic diameter (LVDd) were measured to monitor the improvement of global myocardial contractile function. Myocardial tissue was stained with hematoxylin and eosine (HE) to evaluate the elaborate general morphology of the ischemic myocardium. From morphologic observation and echocardiography in rat heart, aFGF-HMB had suitable size distribution, physical stability and good acoustic resonance function. From AMI rat experiments, aFGF-HMB under US-mediated cavitation technique exerted aFGF cardio protective effect in ischemic myocardium. From histological evaluation, US-mediated cavitation of aFGF-HMB showed improvement of myocardial ischemia. With the visual imaging and US-triggered drug release advantages, US-mediated cavitation of aFGF-HMB might be developed as a novel technique for targeting delivery of aFGF into ischemic myocardium.

Impact of left atrial volume in prediction of outcome after cardiac resynchronization therapy.

UNLABELLED: Left atrial volume index (LAVI) as a predictor of mortality has not been well investigated in patients with cardiac resynchronization therapy (CRT). The purpose of this study is to evaluate the impact of LAVI in predicting mortality in CRT patients. METHODS: We studied 100 consecutive patients who received CRT (male 73, age 69.9 ± 9.6 years). The follow-up duration of all echocardiographic measurements was 14.4 ± 10.5 months after CRT. LAVI was measured from apical views on two-dimensional echocardiography by bi-plane rule. A decrease of left ventricular end systolic volume ≥ 15% after CRT was defined as a positive response to CRT. RESULTS: The mean LAVI at baseline was 59.9 ± 22.7 ml/m(2). LAVI in patients who died (78.2 ± 27.5 ml/m(2)) was significantly greater than those who survived (55.9 ± 19.5 ml/m(2), p<0.0001) during follow-up of 17 ± 10.6 months. The area under ROC curve (AUC) for LAVI predicting death was 0.77 (p=0.0001). The cutoff point for LAVI predicting death was LAVI>59.4 ml/m(2). LAVI>59.4 ml/m(2) was related to mortality by Cox proportional univariate regression [hazard ratio (HR)=5.15, 95% CI=1.48-17.93, p=0.01]. After adjustment for the variables with significant difference by univariate regression, LAVI>59.4 ml/m(2) was continuously related to mortality by multivariate regression (HR=4.56, 95% CI, 1.30-15.97, p=0.02). LAVI>59.4 ml/m(2) was associated with a near 5-fold increase in mortality during follow-up of 17 ± 10.6 months. CONCLUSION: Patients who have LAVI>59.4 ml/m(2) continue to have increased mortality despite CRT.

Thoracic aortic atheroma severity predicts high-risk coronary anatomy in patients undergoing transesophageal echocardiography.

INTRODUCTION: We hypothesized a relationship between severity of thoracic aortic atheroma (AA) and prevalence of high-risk coronary anatomy (HRCA). MATERIAL AND METHODS: We investigated AA diagnosed by transesophageal echocardiography and HRCA diagnosed by coronary angiography in 187 patients. HRCA was defined as ≥ 50% stenosis of the left main coronary artery or significant 3-vessel coronary artery disease (≥ 70% narrowing). RESULTS: HRCA was present in 45 of 187 patients (24%). AA severity was grade I in 55 patients (29%), grade II in 71 patients (38%), grade III in 52 patients (28%), grade IV in 5 patients (3%), and grade V in 4 patients (2%). The area under receiver operating characteristic curve for AA grade predicting HRCA was 0.83 (p = 0.0001). The cut-off points of AA to predict HRCA was > II grade. The sensitivity and specificity of AA > grade II to predict HRCA were 76% and 81%, respectively. After adjustment for 10 variables with significant differences by univariate regression, AA > grade II was related to HRCA by multivariate regression (odds ratio = 7.5, p< 0.0001). During 41-month follow-up, 15 of 61 patients (25%) with AA >grade II and 10 of 126 patients (8%) with AA grade ≤ 2 died (p= 0.004). Survival by Kaplan-Meier plot in patients with AA > grade II was significantly decreased compared to patients with AA ≤ grade II (p= 0.002). CONCLUSIONS: AA > grade II is associated with a 7.5 times increase in HRCA and with a significant reduction in all-cause mortality.