A combination of plaque components analyzed by integrated backscatter intravascular ultrasound and serum pregnancy-associated plasma protein a levels predict the no-reflow phenomenon during percutaneous coronary intervention.

AIMS: Previous studies reported that integrated backscatter intravascular ultrasound (IB-IVUS) provides high diagnostic accuracy for tissue characterization of coronary plaques and that pregnancy-associated plasma protein A (PAPP-A) could be a marker of adverse cardiac outcome in patients with cardiovascular disease. We examined whether IB-IVUS and PAPP-A levels could predict the incidence of no-reflow during percutaneous coronary intervention (PCI) METHODS AND RESULTS: About 176 consecutive patients (138 men, mean age 68 ± 11 years) who underwent PCI with IB-IVUS were prospectively enrolled. Combined no-reflow, including transient filter no-reflow by using distal protection devices, was observed in 31 patients. The percentages of coronary lipid volume (%LV) analyzed by IB-IVUS and serum PAPP-A were significantly higher in patients with combined no-reflow than normal-reflow. To predict no-reflow, a receiver operating characteristic (ROC) analysis determined cut-off values of %LV as 62% and serum PAPP-A as 7.71 ng/mL. The multivariate logistic regression analysis showed that %LV (hazard ratio 4.5, 95% confidence interval 1.6-13.4, P < 0.01) and PAPP-A (hazard ratio 4.32, 95% confidence interval 1.5-12.7, P < 0.01) were independent predictors of combined no-reflow CONCLUSIONS: %LV analyzed by IB-IVUS and serum PAPP-A levels were closely associated with the coronary no-reflow phenomenon. © 2014 Wiley Periodicals, Inc.

A novel mouse model of aortic valve stenosis induced by direct wire injury.

OBJECTIVE: The response-to-tissue-injury theory is currently the favorite paradigm to investigate valve pathology. To the best of our knowledge, there are currently no in vivo valve injury models. There are few calcific aortic valve stenosis (AVS) models that develop hemodynamically significant stenosis. Here, we investigated the effect of direct mechanical injury on aortic valves in vivo and developed a novel mouse model of calcific AVS. APPROACH AND RESULTS: Aortic valve injury was created by inserting and moving a spring guidewire under echocardiographic guidance into the left ventricle of male C57/BL6 mice via right common carotid artery. Serial echocardiographic measurements revealed that aortic velocity was increased 1 week after injury and persistently increased until 16 weeks after injury. AVS mice showed a higher heart weight/body weight ratio and decreased left ventricular fractioning shortening 4 weeks after injury, compared with sham mice. We found remarkable proliferation of valve leaflets 4 weeks after injury. Proliferative valves showed increased production of reactive oxygen species and expression of inflammatory cytokines and osteochondrogenic factors. Alizarin red staining showed valvular calcification 12 weeks after injury. CONCLUSIONS: We report a novel calcific AVS model to support the response-to-tissue-injury theory. This model may be a valuable tool for analyzing the mechanism of AVS and assessing therapeutic options.

A case of coronary artery compression syndrome resulting from peri-valvular regurgitation and long-standing atrial fibrillation.

A man in his 70s with a history of mitral valve replacement (MVR) and long-standing persistent atrial fibrillation (AF) presented with effort angina. Coronary angiography revealed severe stenosis of the left main coronary artery (LMCA). As it was an emergent case, PCI (percutaneous coronary intervention) was selected for treatment. Intravascular ultrasonography revealed no atherosclerotic lesions in the LMCA. The LMCA was effectively dilated by the drug-eluting stent. No elevation in intracardiac pressure was observed in cardiac catheterization after PCI. Computed tomography scan indicated potential compression of the LMCA by the surrounding structures. In cases of long-standing persistent AF and an enlarged atrium after MVR, the possibility of LMCA stenosis due to anatomical changes should be considered. Learning Objectives: ◾Peri-valvular regurgitation and long-standing persistent atrial fibrillation can potentially cause atrial enlargement.◾Coronary artery stenosis without atherosclerosis can occur due to compression from surrounding structures or shifting of the coronary artery.◾Stent therapy provides a temporary solution and coronary artery bypass grafting or switching should be considered if re-stenosis occurs.

Renal tubulointerstitial damage is associated with short-term cardiovascular events in patients with myocardial infarction.

BACKGROUND: Urinary ß2 microglobulin (U-ß2MG) is a more sensitive and accurate marker of tubulointerstitial damage. The etiology of glomerular damage is related to the occurrence of major adverse cardiovascular events (MACE) in patients with myocardial infarction (MI); however, the prognostic importance of tubulointerstitial damage in patients with ST-segment elevation MI (STEMI) has not been established. The aim of this study was to elucidate whether renal tubulointerstitial damage is associated with the occurrence of MACE in patients after STEMI undergoing percutaneous coronary intervention. METHODS AND RESULTS: The degree of renal tubulointerstitial damage was evaluated by measuring the U-ß2MG level in 89 consecutive STEMI patients. There were 22 MACEs during the follow-up period. Patients with MACE had higher U-ß2MG levels than those without MACE, and the U-ß2MG level was an independent predictor for MACE. A Kaplan-Meier analysis revealed that the group with higher U-ß2MG levels corrected for urinary creatinine was associated with a greater risk for MACE. CONCLUSIONS: An elevated U-ß2MG level was associated with the occurrence of MACE in STEMI patients who underwent PCI. Renal tubulointerstitial damage is therefore considered to be associated with the occurrence of MACE.

Acidic urine is associated with poor prognosis in patients with chronic heart failure.

Renal dysfunction is reported to be associated with poor outcomes in patients with chronic heart failure (CHF). A recent study showed that acidic urine is related to chronic kidney disease, which is a risk factor for the development of CHF. However, it remains to be determined whether acidic urine is associated with poor outcomes in patients with CHF. We measured urine pH using dipsticks in 537 patients with CHF. Acidic urine was defined as urine pH ≤5.5. Patients were prospectively followed during a median follow-up period of 556 days. There were 145 cardiac events. Prevalence of acidic urine was increased with advancing stage of chronic kidney disease. Patients with acidic urine had a more severe New York Heart Association functional class compared with those with normal urine. In the multivariate Cox proportional hazard analysis, acidic urine was independently associated with poor outcomes in patients with CHF after adjustment of confounding factors. A Kaplan-Meier analysis demonstrated that the rate of cardiac events was higher in patients with acidic urine than in those with normal urine. The presence of acidic urine can reliably identify patients at high risk of future cardiac events in patients with CHF.

Circulating heart-type fatty acid binding protein levels predict the occurrence of appropriate shocks and cardiac death in patients with implantable cardioverter-defibrillators.

BACKGROUND: The association between ongoing myocardial damage and outcomes in patients who have received an implantable cardioverter-defibrillator (ICD) is unclear. METHODS AND RESULTS: Consecutive patients with cardiomyopathy, who had received an ICD (n = 107, mean age 65 ± 11 years), were prospectively enrolled. Myocardial membrane injury (heart-type fatty acid binding protein [H-FABP] >4.3 ng/mL) and myofibrillar injury (troponin T >0.01 ng/mL) were defined using receiver operating characteristic curves. Patients were followed for a median of 33.6 months, to an end point of appropriate ICD shock or cardiac death. Myocardial membrane injury (45%) and myofibrillar injury (41%) were equally prevalent among patients with cardiomyopathy who had received ICDs. Appropriate ICD shocks or cardiac death occurred in 31% and 15% of patients, respectively. Multivariate Cox regression analysis showed that serum H-FABP levels >4.3 ng/mL, but not troponin T levels, were a significant independent prognostic factor for cardiac events (hazard ratio 5.502, 95% confidence interval 1.705-17.75, P = .004). Subgroup analysis revealed that measuring H-FABP levels was valuable for anticipating event-free survival among patients with ICDs who were receiving amiodarone. High H-FABP levels also predicted subsequent outcomes in patients who had received ICDs for primary or secondary prevention. CONCLUSION: Evaluating myocardial damage using H-FABP may be a promising tool for predicting outcomes in patients with cardiomyopathy who have received ICDs.

Device troubleshooting: cross connection of ventricular leads in a patient with decreased right ventricular electrical activity.

A patient with cardiac sarcoidosis showed low R-wave amplitude in the entire right ventricle (RV). To troubleshoot this, a left ventricular (LV) lead was implanted in the coronary vein. The pace/sense terminal of the defibrillation lead was connected to LV:IS-1 of the defibrillator. Conversely, the LV lead was connected to RV:IS-1. Induced ventricular fibrillation was successfully terminated without any undersensing.

Increased left atrial volume index predicts a poor prognosis in patients with heart failure.

BACKGROUND: Left atrial volume index (LAVI) is known to reflect the duration and severity of increased left atrial pressure caused by left ventricular (LV) diastolic dysfunction. However, the prognostic value of LAVI in patients with heart failure (HF) has not been fully investigated. METHODS AND RESULTS: Transthoracic echocardiography was performed in 146 consecutive patients (78 men, 68 women; mean age 72 ± 12 y) who were hospitalized for HF. There were 45 cardiac events (32%) during a median follow-up period of 448 days. There were no significant differences in LV end-diastolic dimensions or ejection fraction between patients who did or did not have cardiac events. However, LAVI was markedly higher in patients with, than those without, cardiac events (56 ± 26 vs 44 ± 22 mL/m(2); P < .01). Kaplan-Meier analysis showed that there was a stepwise increase in risk of cardiac events with each increment of LAVI category, and LAVI >53.3 mL/m(2) correlated with the highest risk of cardiac events (log-rank test; P < .01). Multivariate Cox proportional hazard analysis showed that high LAVI was an independent predictor for cardiac events (hazard ratio 1.427; 95% confidence interval 1.024-1.934; P < .05). CONCLUSION: LAVI may be useful for stratification of risk in patients with HF.

8-Hydroxy-2'-deoxyguanosine is a prognostic mediator for cardiac event.

BACKGROUND: DNA in the nucleus is one of the major targets of reactive oxygen species (ROS), and oxidative DNA damage has been implicated in the pathogenesis of chronic heart failure. 8-Hydroxy-2'-deoxyguanosine (8-OHdG) is produced from deoxyguanosine in DNA by ROS. The purpose of this present study was to examine the clinical significance of serum 8-OHdG levels in patients with heart failure. METHODS: We measured serum 8-OHdG levels in 230 patients with chronic heart failure and 42 control subjects without heart failure by sandwich enzyme-linked immunosorbent assay. Patients were prospectively followed during a median follow-up period of 472 days with the end points of cardiac death or progressive heart failure requiring re-hospitalization. RESULTS: Serum 8-OHdG concentrations were higher in patients with heart failure than in control subjects (P < 0·001) and increased with advancing New York Heart Association (NYHA) functional class (P < 0·001). Normal upper limit of 8-OHdG level was determined as mean ± 2SD value from 42 control subjects (0·40 ng mL(-1)). Abnormally high serum 8-OHdG levels (> 0·40 ng mL(-1)) were observed in 21·2%, 43·1%, 42·6% and 69·4% through NYHA I to IV (P < 0·001). A total of 66 cardiac events occurred during a follow-up period, and Kaplan-Meier survival curves demonstrated that cardiac event rate was markedly higher in patients with high 8-OHdG levels than in those with normal 8-OHdG levels (62·4% vs. 29·6%, P = 0·0007). CONCLUSIONS: Serum 8-OHdG levels provide important prognostic information for the risk stratification of patients with heart failure.

Persistent abnormal value of late potential in Brugada syndrome associated with hypokalemia.

Hypokalemia accentuates the electrocardiographic (ECG) pattern of Brugada syndrome. We report two patients with Brugada syndrome and hypokalemia-induced lethal events. Despite concealing the typical ECG pattern with normalization of serum potassium levels, late potentials were persistently detected by signal-averaged ECG, even at the 18-month follow-up. An implantable cardioverter defibrillator was inserted to prevent sudden cardiac death.

Suppressive effects of valsartan on microalbuminuria and CRP in patients with metabolic syndrome (Val-Mets).

The presence of metabolic syndrome (Mets) increases the risk for cardiovascular disease. There is a significant correlation between the levels of urinary albumin to creatinine ratio (UACR) and high-sensitive C-reactive peptide (hs-CRP), and accumulation of each Mets component. Increasing evidence has shown the importance of blockade of renin-angiotensin-systems (RAS) for reducing urinary albumin excretion and hs-CRP levels in Mets patients. However, the impact of RAS blockade on these effects in hypertensive (HT) Mets patients without diabetes mellitus (DM) has not been evaluated. We prospectively measured the levels of UACR and hs-CRP in 153 HT patients with and without Mets. Body weight; waist circumference; presence of dyslipidemia and DM, and levels of HOMA-R, UACR, and hs-CRP were significantly higher in HT patients with Mets than in those without Mets. After we treated these Mets patients with valsartan for 6 months, blood pressure (BP), UACR, and hs-CRP were decreased, whereas body weight, HOMR-R, and the lipid profile were not changed. In HT Mets patients without DM, 6 months after valsartan administration, levels of UACR and hs-CRP were also significantly decreased by 37.8% (-9.0-56.5%, p < 0.05) and 23.6% (-28.7-73.4%, p < 0.05), respectively. However, the percentage change of UACR and hs-CRP was not correlated with the reduction in BP. Valsartan administration lowered increased levels of chronic inflammation in both HT Mets patients with DM and in those without DM. These results indicate that the anti-inflammatory properties of valsartan might also have beneficial effects in Mets patients without DM.

Serum midkine as a predictor of cardiac events in patients with chronic heart failure.

BACKGROUND: Midkine, a heparin-binding growth factor, has various functions such as migration of inflammatory cell and anti-apoptotic effect. Invasion of inflammatory cell and cardiomyocyte apoptosis are involved in development and progression of heart failure (HF). However, the relationship between midkine and HF has not been previously examined. Therefore, we examined clinical significance of serum midkine levels to determine the prognosis of HF patients. METHODS AND RESULTS: Serum levels of midkine were measured at admission in 216 consecutive patients hospitalized for HF and 60 control subjects. Patients were prospectively followed during a mean follow-up period of 653 +/- 375 days with the end points of cardiac death and progressive HF requiring rehospitalization. Serum concentrations of midkine were significantly higher in patients with HF than in controls. Patients with cardiac events had significantly higher concentrations of midkine than those without cardiac events. Kaplan-Meier analysis revealed that cardiac event rates increased markedly as midkine levels rose. Furthermore in the multivariate analysis, after adjustment for age, gender ,and complications, midkine was the independent predictor of cardiac events. CONCLUSION: Serum midkine levels are increased in HF patients, and midkine is a novel marker for risk stratifying HF patients.

Relation of serum heat shock protein 60 level to severity and prognosis in chronic heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Heat shock protein (HSP) 60 is induced by a variety of stressors, including oxidative stress and inflammation, and it plays a protective role against stress-induced cardiomyocyte injury. Recently, it has been reported that HSP 60 exists in the circulation. Chronic heart failure (CHF) is characterized by systemic abnormalities, and the myocardium is exposed to various stressors. However, the clinical significance of serum HSP 60 has not been examined in CHF. Therefore, the purpose of this study was to examine whether HSP 60 is correlated with the severity of CHF and whether HSP 60 can predict clinical outcomes in patients with CHF. Serum HSP 60 levels were measured in 112 patients with CHF and 62 control subjects. Serum HSP 60 levels were higher in patients with CHF than in control subjects and increased with advancing New York Heart Association functional class. There were 37 cardiac events during a mean follow-up period of 569 +/- 476 days (range 17 to 1,986). Serum HSP 60 levels were higher in patients with cardiac events than in event-free patients. Patients were divided into 4 groups on the basis of HSP 60 level. Cox proportional-hazards regression analysis and Kaplan-Meier analysis revealed that the fourth quartile was associated with the greatest risk for cardiac events. In conclusion, serum HSP 60 level was related to the severity of CHF and associated with a high risk for adverse cardiac events in patients CHF.

A randomized controlled trial of eicosapentaenoic acid in patients with coronary heart disease on statins.

BACKGROUND: There is a residual risk of coronary heart disease (CHD) despite intensive statin therapy for secondary prevention. The aim of this study was to investigate whether coronary plaque regression and stabilization are reinforced by the addition of eicosapentaenoic acid (EPA) to high-dose pitavastatin (PTV). METHODS: We enrolled 193 CHD patients who underwent percutaneous coronary intervention (PCI) in six hospitals. Patients were randomly allocated to the PTV group (PTV 4mg/day, n=96) or PTV/EPA group (PTV 4mg/day and EPA 1800mg/day, n=97), and prospectively followed for 6-8 months. Coronary plaque volume and composition in nonstenting lesions were analyzed by integrated backscatter intravascular ultrasound (IB-IVUS). RESULTS: The PTV/EPA group showed a greater reduction in total atheroma volume compared to PTV group. IB-IVUS analyses revealed that lipid volume was significantly decreased during follow-up period in only PTV/EPA group. The efficacy of additional EPA therapy on lipid volume reduction was significantly higher in stable angina pectoris (SAP) patients compared to acute coronary syndrome patients. EPA/AA ratio was significantly improved in PTV/EPA group compared to PTV group. There was no significant difference in the incidence of major adverse cardiovascular events and side effects. CONCLUSIONS: Combination EPA/PTV therapy significantly reduced coronary plaque volume compared to PTV therapy alone. Plaque stabilization was also reinforced by EPA/PTV therapy in particular SAP patients. The addition of EPA is a promising option to reduce residual CHD risk under intensive statin therapy.

Impact of Serum Uric Acid Levels on Coronary Plaque Stability Evaluated Using Integrated Backscatter Intravascular Ultrasound in Patients with Coronary Artery Disease.

AIM: Because the prevalence of hyperuricemia is lower in females than in males, the association between hyperuricemia and cardiovascular disease has been frequently reported in females. Increased serum uric acid levels are associated with the presence of cardiovascular risk factors such as hypertension, renal dysfunction, insulin resistance, and metabolic syndrome. However, it is controversial whether hyperuricemia is an independent risk factor for coronary artery disease in both the genders. The purpose of this study was to investigate the relationship between serum uric acid levels and coronary plaque components assessed using integrated backscatter intravascular ultrasound (IB-IVUS) in males and females. METHODS: In total, 385 patients (298 males and 87 females) who underwent percutaneous coronary intervention using IB-IVUS were divided into three groups in each gender according to their serum uric acid levels. We characterized tissue from coronary plaques in culprit lesions. RESULTS: Serum uric acid levels significantly correlated with percent lipid volume (r=0.37) and inversely correlated with percent fibrous volume (r=－0.35). Multivariate analysis showed that the uric acid level was independently associated with lipid-rich plaques (odds ratio 2.43, 95%, confidence interval 1.75-3.47). The prevalence of lipid-rich plaques increased with increasing uric acid levels in both genders. CONCLUSION: Increased serum uric acid levels were associated with larger lipid content plaques in both genders.

Ongoing myocardial damage relates to cardiac sympathetic nervous disintegrity in patients with heart failure.

UNLABELLED: Iodine-123-metaiodobenzylguanidine (123I-MIBG) has been used to assess the integrity and function of the cardiac sympathetic nervous system in patients with heart failure. Heart-type fatty acid binding protein (H-FABP) is released into the circulation when the myocardium is injured, and H-FABP has been recently used as a novel marker for the diagnosis of ongoing myocardial damage. OBJECTIVE: The aim of the present study was to compare cardiac sympathetic nervous activity assessed by 123I-MIBG imaging with serum levels of H-FABP in patients with heart failure. METHODS: Fifty patients with chronic heart failure were studied. 123I-MIBG imaging was carried out at 30 min (early) and 240 min (delayed) after the tracer injection. We measured serum levels of H-FABP using a sandwich enzyme linked immunosorbent assay. RESULTS: Heart to mediastinum (H/M) ratios of 123I-MIBG decreased and washout rate increased with higher New York Heart Association (NYHA) functional class. H-FABP, norepinephrine and brain natriuretic peptide (BNP) levels increased as the severity of NYHA class advanced. Delayed H/M ratio was significantly correlated with H-FABP (r = -0.296, p = 0.029) and BNP (r = -0.335, p = 0.0213). Myocardial washout rate of 123I-MIBG was also correlated with H-FABP (r = 0.469, p < 0.001), norepinephrine (r = 0.433, p = 0.005), and BNP (r = 0.465, p = 0.001). CONCLUSIONS: These data suggest that cardiac sympathetic nervous activation was associated with ongoing cardiomyocyte damage characterized by an elevated serum level of H-FABP in patients with heart failure. 123I-MIBG imaging is an appropriate approach to evaluate non-invasively not only cardiac sympathetic nervous activity, but also latent ongoing myocardial damage in the failing heart.

Deficiency of Long Pentraxin PTX3 Promoted Neointimal Hyperplasia after Vascular Injury.

AIM: Pentraxin 3 (PTX3) is a novel marker for the primary local activation of innate immunity and inflammatory responses. Although clinical and experimental evidence suggests that PTX3 is associated with atherosclerosis, the relationship between PTX3 and vascular remodeling after wall injury remains to be determined. We investigated the effects of PTX3 on neointimal hyperplasia following wire vascular injury. METHODS: PTX3 systemic knockout (PTX3-KO) mice and wild-type littermate (WT) mice were subjected to wire-mediated endovascular injury. At four weeks after wire-mediated injury, the areas of neointimal and medial hyperplasia were evaluated. RESULTS: The PTX3-KO mice exhibited higher hyperplasia/media ratios than the WT mice after wire injury, and the degree of Mac-3-positive macrophage accumulation was significantly higher in the PTX3-KO mice than in the WT mice. Furthermore, the PTX3-KO mice showed a much greater increase in the number of PCNA-stained cells in the vascular wall than that observed in the WT mice. CONCLUSIONS: A deficiency of PTX3 results in deteriorated neointimal hyperplasia after vascular injury via the effects of macrophage accumulation and vascular smooth muscle cell proliferation and migration.

Role of epicardial adipose tissue in coronary artery disease in non-obese patients.

BACKGROUND: Epicardial adipose tissue (EAT) surrounding the heart may contribute to the development of coronary artery disease (CAD) through its local secretion of adipocytokines. Although the quantity of EAT is associated with obesity and metabolic syndrome, the role of EAT in the development of CAD in non-obese patients remains to be determined. METHODS: This study included 41 patients with CAD who underwent coronary artery bypass graft surgery and 28 patients without CAD who underwent other cardiac surgery. EAT volume was measured by 64-slice multi-detector computed tomography before the surgery. We obtained pericardial fluid and epicardial and subcutaneous adipose tissue samples at the surgery. We investigated the relationship between EAT volume and adiponectin levels in pericardial fluid and incident CAD in patients with and without obesity (body mass index>25 kg/m(2)). RESULTS: There was no significant difference in EAT volume between obese patients with and without CAD (55.5 ± 40.2 mL vs. 40.1 ± 19.7 mL, p=0.323). However, EAT volume was significantly greater in non-obese patients with CAD compared to those without CAD (35.0 ± 18.8 mL vs. 15.7 ± 11.0 mL, p<0.001). Adiponectin concentrations in pericardial fluid were significantly lower in non-obese patients with CAD compared to those without CAD (2.7 ± 2.0 µg/mL vs. 4.3 ± 3.7 µg/mL, p=0.049), whereas the adiponectin levels were decreased in obese patients regardless of the presence of CAD. Non-obese patients with CAD had significantly larger size adipocytes in EAT but not subcutaneous adipose tissue compared to those without CAD. Multiple logistic regression analysis showed that increased EAT volume was independently associated with incident CAD in non-obese patients. CONCLUSION: Increased EAT may play a crucial role in development of CAD through impairment of adiponectin secretion in non-obese patients.

Prognostic value of myocardial damage markers in patients with chronic heart failure with atrial fibrillation.

OBJECTIVE: The aim of the present study was to examine the relationship between myocardial damage caused by atrial fibrillation (AF) and subsequent cardiovascular events in AF patients with chronic heart failure (CHF). METHODS AND RESULTS: We measured the serum levels of heart-type fatty acid binding protein (H-FABP) and high-sensitivity troponin T in 402 consecutive CHF patients with chronic AF (CHF-AF, n=201) or sinus rhythm (CHF-SR, n=201). The patients with CHF-AF had higher H-FABP and troponin T levels than those with CHF-SR. In order to examine the prognostic value of myocardial damage markers in CHF-AF and CHF-SR patients, we followed the above patients and analyzed their clinical outcomes. A multivariate Cox proportional hazard analysis revealed that both the serum H-FABP and troponin T levels independently predicted subsequent cardiovascular events. A Kaplan-Meier analysis demonstrated that the rate of cardiovascular events was higher in the patients with elevated H-FABP and troponin T levels. The optimal cut-off values for the myocardial damage markers of cardiovascular events were higher in the CHF-AF patients than in the CHF-SR patients (H-FABP, 5.4 vs. 4.6 ng/mL and troponin T, 0.030 vs. 0.013 ng/mL). CONCLUSION: Myocardial damage advances in association with the presence of AF and is associated with subsequent cardiovascular events in both CHF-AF and CHF-SR patients. In this study, the cut-off values for the myocardial damage markers were higher in the CHF-AF patients than in the CHF-SR patients.

Electrocardiographic left ventricular hypertrophy Cornell product is a feasible predictor of cardiac prognosis in patients with chronic heart failure.

BACKGROUND: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular disease and is associated with heart failure development. The Cornell product is an easily measured electrocardiographic parameter for assessing LVH. However, it is undetermined whether the Cornell product can predict the cardiac prognosis of chronic heart failure (CHF) patients. METHODS AND RESULTS: We performed standard 12-lead electrocardiography and calculated the Cornell product in 432 consecutive CHF patients. LV geometry was assessed as normal, concentric remodeling, concentric or eccentric hypertrophy. The Cornell product was significantly higher in patients with eccentric hypertrophy, and increased with advancing New York Heart Association functional class. During a median follow-up of 660 days, there were 121 cardiac events including 36 cardiac deaths and 85 re-hospitalizations for worsening heart failure. Multivariate Cox proportional hazard analysis showed that the Cornell product was an independent predictor of cardiac events in CHF patients. Patients in the highest quartile of Cornell product had a higher prevalence of LV eccentric hypertrophy (22, 29, 33 and 67 % for quartiles one through four). Kaplan-Meier analysis demonstrated that the highest quartile of Cornell product was associated with the greatest risk among CHF patients. CONCLUSION: The Cornell product is associated with LV eccentric hypertrophy and can be used to predict future cardiac events in CHF patients.