Prolonged total atrial conduction time evaluated with tissue Doppler imaging predicts poor cardiac prognosis in patients with heart failure.

Prolonged total atrial conduction time is caused by atrial remodeling. Left atrial remodeling is associated with poor outcome in patients with heart failure (HF). This study aimed to investigate whether prolonged total atrial conduction time predicts poor prognosis in patients with HF. We performed transthoracic echocardiography in 100 patients (65 men; mean age 68 ± 13 years) who were hospitalized for HF. Total atrial conduction time was defined as the duration from P wave onset on electrocardiography to peak A' wave on tissue Doppler imaging (TDI) echocardiography (PA-TDI duration). There were 37 cardiac events (37%) during a median follow-up period of 414 days. The PATDI duration was significantly longer in patients with cardiac events than in those without (150 ± 18 ms vs 133 ± 19 ms; P < 0.05). There were no significant differences in left ventricular end-diastolic dimensions and ejection fractions between patients with and without cardiac events. Patients with HF were divided into 3 groups according to tertiles of the PA-TDI duration. Kaplan-Meier analysis showed that the highest tertile of PA-TDI duration was associated with the greatest risk among patients with HF. Multivariate Cox proportional hazard analysis showed that the PA-TDI duration was an independent predictor of cardiac events, leading to the conclusion that prolonged PA-TDI duration was a feasible predictor of cardiac prognosis in patients with HF.

Serum carboxy-terminal telopeptide of type I collagen (I-CTP) is predictive of clinical outcome in peripheral artery disease patients following endovascular therapy.

Peripheral artery disease (PAD) is a risk factor for the development of heart failure and mortality. The serum levels of carboxy-terminal telopeptide of type I collagen (I-CTP), a marker for collagen degradation derived from the extracellular matrix of vascular and myocardial tissue, is reportedly a useful marker for cardiac events in patients with heart disease. However, it remains unclear whether I-CTP can predict poor clinical outcome in patients with PAD. Serum I-CTP was measured in 246 consecutive PAD patients who underwent endovascular therapy. Patients were prospectively followed during a median follow-up period of 887 days with the end points of major adverse cardiovascular events (MACE). I-CTP was significantly higher in patients with critical limb ischemia than those without. A multivariate Cox proportional hazard analysis revealed that I-CTP was an independent predictor of MACE after adjusting for confounding factors. Patients were stratified into three groups based on I-CTP level tertile, and those with third tertile had higher levels of brain natriuretic peptide levels and high-sensitivity C-reactive protein compared to the other two groups. Kaplan-Meier analysis demonstrated that patients in the highest tertile of I-CTP also had the greatest risk of MACE. The net reclassification index significantly improved with the addition of I-CTP to basic predictors. I-CTP is a reliable marker and indicator for MACE in patients with PAD.

Cystatin C-based eGFR is a superior prognostic parameter to creatinine-based eGFR in post-endovascular therapy peripheral artery disease patients.

BACKGROUND: Kidney dysfunction is reportedly associated with adverse outcome in patients with peripheral artery disease (PAD). Estimated glomerular filtration rate (eGFR), a recently popularized index for assessing kidney function, is calculated using serum creatinine or cystatin C. Compared with creatinine-based eGFR (eGFRcr), cystatin C-based eGFR (eGFRcys) is less affected by age, gender, and muscle mass. We hypothesized that eGFRcys is a feasible prognostic biomarker despite muscle sarcopenia in patients with PAD. METHODS AND RESULTS: We calculated both eGFRcr and eGFRcys according to the Kidney Disease: Improving Global Outcomes (KDIGO) guideline in 234 PAD patients who underwent endovascular therapy. Patients were prospectively followed during a median follow-up period of 964 days for the endpoint of major adverse cardiovascular and cerebrovascular events (MACCE). On multivariate Cox proportional hazard analysis eGFRcys, but not eGFRcr, was an independent predictor of MACCE. The C index was larger for eGFRcys than eGFRcr (0.69 vs. 0.57, P=0.0006). On Kaplan-Meier analysis the incidence of MACCE was increased with advancing chronic kidney disease stage based on eGFRcys, but not on eGFRcr, in patients with PAD. Net reclassification index was improved with the addition of eGFRcys to basic predictors. CONCLUSIONS: Compared with eGFRcr, eGFRcys may be a more reliable biomarker for MACCE and patient risk stratification.

Renal tubular damage is associated with poor clinical outcome in patients with peripheral artery disease who underwent endovascular therapy.

BACKGROUND: Kidney dysfunction is associated with adverse outcome in patients with peripheral artery disease (PAD). Renal tubulointerstitial damage (RTD) is another type of kidney dysfunction from glomerular damage. RTD is reported to be a risk for future cardiac event in patients with heart disease. However, it remains to be determined whether RTD is predictive of poor clinical outcome in patients with PAD. METHODS AND RESULTS: RTD markers (urinary N-acetyl-ß-D-glucosamidase; NAG and urinary ß-2 microglobulin to creatinine ratio) and Glomerular damage markers (cystatin C-based estimated glomerular filtration rate, proteinuria, and microalbuminuria) were measured in 265 consecutive PAD patients who underwent endovascular therapy. Patients were prospectively followed for a median length of 804days, with end points of major adverse cardiovascular and cerebrovascular events (MACCE). Overall, 73% of patients exhibited excess urinary NAG excretion, and values were higher in patients with critical limb ischemia. A multivariate Cox proportional hazard analysis revealed that NAG was an independent predictor of MACCE. When patients were divided according to NAG level, Kaplan-Meier analysis demonstrated that the third tertile was associated with the greatest risk for MACCE. The C index in NAG was the greatest among kidney dysfunction markers. Moreover, the net reclassification index was improved by the addition of NAG to basic predictors including glomerular damage markers. CONCLUSION: RTD is common and associated with disease severity and clinical outcome in patients with PAD, indicating that it could be the additional clinical information to glomerular damage in patients with PAD.

Heart-type fatty acid binding protein and high-sensitivity troponin T are myocardial damage markers that could predict adverse clinical outcomes in patients with peripheral artery disease.

BACKGROUND: Despite many recent advances in endovascular therapy (EVT), peripheral artery disease (PAD) is an increasing health problem with high mortality. Heart-type fatty acid-binding protein (H-FABP) and high-sensitivity troponin T (hsTnT) are markers of ongoing myocardial damage and have been reported to be useful indicators of future cardiovascular events. However, it remains to be determined whether H-FABP and hsTnT can predict adverse clinical outcomes in patients with PAD. METHODS AND RESULTS: We enrolled 208 de novo PAD patients who underwent EVT. Serum H-FABP and hsTnT were measured in all patients before EVT. During the median follow-up period of 694 days, there were 40 major adverse cardiovascular and cerebrovascular events (MACCEs) including all-cause deaths, and re-hospitalizations due to cardiovascular and cerebrovascular diseases and amputations. H-FABP and hsTnT were found to be higher in patients with critical limb ischemia (CLI) compared to those without this condition. Multivariate Cox proportional hazard regression analysis revealed that both H-FABP and hsTnT were independent predictors of MACCEs after adjustment for confounding factors. Kaplan-Meier analysis demonstrated that patients in the highest tertile according to H-FABP levels, as well as those in the highest hsTnT tertile, were at greatest risk for MACCEs. The net reclassification index was significantly improved by the addition of H-FABP as well as the addition of hsTnT to traditional risk factors. CONCLUSION: The myocardial damage markers H-FABP and hsTnT were increased in PAD patients with CLI and could predict MACCEs in PAD patients.

Left atrial strain as evaluated by two-dimensional speckle tracking predicts left atrial appendage dysfunction in patients with acute ischemic stroke.

BACKGROUND: Left atrial appendage (LAA) dysfunction predisposes patients with atrial fibrillation (AF) to cardioembolic stroke. Two-dimensional (2D) speckle tracking was reported to be useful for evaluating left atrial (LA) regional function, as well as left ventricular function. However, it remains unclear whether 2D speckle tracking is useful for evaluating LAA dysfunction. Therefore, we investigated whether decreased LA strain may predict LAA dysfunction and thrombus formation in patients with acute ischemic stroke. METHODS: We performed transthoracic and transesophageal echocardiography in 120 patients (83 males, mean age 72 ± 11 years) within 7 days of onset of an acute ischemic stroke. Longitudinal LA strain was evaluated using 2D speckle tracking imaging at each LA segment, and peak systolic strain was calculated by averaging the results for each segment. RESULTS: Forty-eight patients had LAA dysfunction as defined by the presence of LAA thrombus and/or severe spontaneous echo contrast. LA peak systolic strain was significantly decreased in patients with LAA dysfunction compared to those without (32.3 ± 13.7% vs. 12.1 ± 7.2%, p < 0.0001). LA peak systolic strain was significantly correlated with LAA emptying flow velocity (r = 0.693, p < 0.0001). The optimum LA peak systolic strain cut-off value for predicting LAA dysfunction was 19%. Multivariate logistic regression analysis showed that LA peak systolic strain was an independent predictor of LAA dysfunction (odds ratio 0.059, 95% confidence interval 0.018-0.146; p < 0.0001). CONCLUSION: Decreased LA peak systolic strain was independently associated with LAA dysfunction in patients with acute ischemic stroke.