Effects of hyperaemia on left ventricular longitudinal strain in patients with suspected coronary artery disease : A first-pass stress perfusion cardiovascular magnetic resonance imaging study.

AIMS: Myocardial perfusion imaging during hyperaemic stress is commonly used to detect coronary artery disease. The aim of this study was to investigate the relationship between left ventricular global longitudinal strain (GLS), strain rate (GLSR), myocardial early (E') and late diastolic velocities (A') with adenosine stress first-pass perfusion cardiovascular magnetic resonance (CMR) imaging. METHODS AND RESULTS: 44 patients met the inclusion criteria and underwent CMR imaging. The CMR imaging protocol included: rest/stress horizontal long-axis (HLA) cine, rest/stress first-pass adenosine perfusion and late gadolinium enhancement imaging. Rest and stress HLA cine CMR images were analysed using feature-tracking software for the assessment of myocardial deformation. The presence of perfusion defects was scored on a binomial scale. In patients with hyperaemia-induced perfusion defects, rest global longitudinal strain GLS (-16.9 ± 3.7 vs. -19.6 ± 3.4; p-value = 0.02), E' (-86 ± 22 vs. -109 ± 38; p-value = 0.02), GLSR (69 ± 31 vs. 93 ± 38; p-value = 0.01) and stress GLS (-16.5 ± 4 vs. -21 ± 3.1; p < 0.001) were significantly reduced when compared with patients with no perfusion defects. Stress GLS was the strongest independent predictor of perfusion defects (odds ratio 1.43 95% confidence interval 1.14-1.78, p-value <0.001). A threshold of -19.8% for stress GLS demonstrated 78% sensitivity and 73% specificity for the presence of hyperaemia-induced perfusion defects. CONCLUSIONS: At peak myocardial hyperaemic stress, GLS is reduced in the presence of a perfusion defect in patients with suspected coronary artery disease. This reduction is most likely caused by reduced endocardial blood flow at maximal hyperaemia because of transmural redistribution of blood flow in the presence of significant coronary stenosis.

Use of copeptin and high-sensitive cardiac troponin T for diagnosis and prognosis in patients with diabetes mellitus and suspected acute myocardial infarction.

BACKGROUND: Diabetes is a major risk factor for acute myocardial infarction (AMI). Assessment of diabetic patients is challenging due to an often atypical presentation of symptoms. We aimed to evaluate the two novel biomarkers copeptin and high-sensitive cardiac troponin (hs-TnT) for the improvement of early diagnosis and risk-stratification in patients with diabetes and suspected AMI. METHODS: In this prospective international multicenter study we evaluated 379 patients with diabetes in a cohort of 1991 patients presenting with symptoms suggestive of AMI. The measurement of biomarkers was performed at presentation. RESULTS: Among the 379 diabetic patients, 32.7% had AMI, and in the 1621 patients without diabetes, 18.8% had AMI. The additional use of copeptin improved the diagnostic accuracy provided by conventional troponin alone (AUC 0.86 vs. 0.79, p=0.004). During a median follow-up of 814 days, 49 (13.1%) diabetic patients died. Cumulative 2-year survival rate for patients with copeptin levels below 9 pmol/l was 96.6% compared to 82.8% in patients above that level (p<0.001). The same was observed for hs-TnT with a cutoff level of 14 ng/l (97.7% vs. 82.0%, p<0.001) respective of cTnT with a cutoff level of 10 ng/l (93.5% vs. 75.6%, p<0.001). In multivariate Cox analysis, copeptin, hs-TnT and cTnT were strong and independent predictors of 24-month-mortality. Using the dual marker strategy (copeptin and troponin) identified two groups of high-risk patients where 22.5% of the group with hs-cTnT and copeptin above the cutoff and 28.6% with cTnT and copeptin above the cutoff died. CONCLUSION: In diabetic patients, copeptin only slightly improves the early diagnosis of AMI provided by hs-cTnT. However, both markers (copeptin and troponin) predict long-term mortality accurately and independently of each other.

Diagnostic and prognostic value of circulating microRNAs in patients with acute chest pain.

OBJECTIVES: To address the diagnostic value of circulating microRNAs (miRNAs) in patients presenting with acute chest pain. DESIGN: In a prospective, international, multicentre study, six miRNAs (miR-133a, miR-208b, miR-223, miR-320a, miR-451 and miR-499) were simultaneously measured in a blinded fashion in 1155 unselected patients presenting with acute chest pain to the emergency department. The final diagnosis was adjudicated by two independent cardiologists. The clinical follow-up period was 2 years. RESULTS: Acute myocardial infarction (AMI) was the adjudicated final diagnosis in 224 patients (19%). Levels of miR-208b, miR-499 and miR-320a were significantly higher in patients with AMI compared to those with other final diagnoses. MiR-208b provided the highest diagnostic accuracy for AMI (area under the receiver operating characteristic curve 0.76, 95% confidence interval 0.72-0.80). This diagnostic value was lower than that of the fourth-generation cardiac troponin T (cTnT; 0.84) or the high-sensitivity cTnT (hs-cTnT; 0.94; both P < 0.001 for comparison). None of the six miRNAs provided added diagnostic value when combined with cTnT or hs-cTnT (ns for the comparison of combinations vs. cTnT or hs-cTnT alone). During follow-up, 102 (9%) patients died. Levels of MiR-208b were higher in patients who died within 30 days, but the prognostic accuracy was low to moderate. None of the miRNAs predicted long-term mortality. CONCLUSION: The miRNAs investigated in this study do not seem to provide incremental diagnostic or prognostic value in patients presenting with suspected AMI.

Sensitive cardiac troponin in the diagnosis and risk stratification of acute heart failure.

BACKGROUND: The aim of our study was to investigate the diagnostic and prognostic value of a sensitive cardiac troponin I (s-cTnI) assay in patients with acute heart failure (AHF). METHODS: Sensitive cardiac troponin I was measured in 667 consecutive patients at presentation to the emergency department with acute dyspnoea. Three s-cTnI strata were predefined: below the limit of detection (<0.01 µg L(-1) , undetectable), detectable but still within the normal range (0.01-0.027 µg L(-1) ) and increased (≥0.028 µg L(-1) , ≥99th percentile). The final diagnosis was adjudicated by two independent cardiologists blinded to the s-cTnI levels. Median follow-up in patients with AHF was 371 days. RESULTS: Levels of s-cTnI were higher in patients with AHF (n = 377, 57%) compared to patients with noncardiac causes of acute dyspnoea (median 0.02 vs. <0.01 µg L(-1) , P < 0.001). In patients with AHF, in-hospital mortality increased with increasing s-cTnI in the three strata (2%, 5% and 14%, P < 0.001). One-year mortality also increased with increasing s-cTnI (21%, 33% and 47%, P < 0.001). s-cTnI remained an independent predictor of 1-year mortality [adjusted odds ratio 1.03 for each increase of 0.1 µg L(-1) , 95% confidence interval (CI) 1.02-1.05, P < 0.001] after adjustment for other risk factors including B-type natriuretic peptide. The net reclassification improvement was 68% (P < 0.001), and absolute integrated discrimination improvement was 0.18 (P < 0.001). The diagnostic accuracy of s-cTnI for the diagnosis of AHF as quantified by the area under the receiver operating characteristic curve was 0.78 (95% CI, 0.75-0.82). CONCLUSIONS: Sensitive cardiac troponin I is a strong predictor of short- and long-term prognosis in AHF that helps to reclassify patients in terms of mortality risk. Detectable levels of s-cTnI, even within the normal range, are independently associated with mortality.

A novel pulse duplicator system: evaluation of different valve prostheses.

BACKGROUND: The hemodynamic characteristics of different heart valve prostheses have been investigated in vitro with a novel pulse duplicator. A novel valved stent for transapical or percutaneous valve implantation has been compared with a native heart valve and mechanical heart valves. METHODS: All experiments were designed to imitate both physiologic pressure ratios and flow characteristics in diastole and systole. After calibrating the system using a human aortic valve (primary orifice diameter: 22.0 mm), the following valves were studied under aortic pulsatile flow conditions: Hall-Kaster (Medtronic-Hall, 20.0 mm), St. Jude Medical (20.0 mm), a newly developed tricuspid valved stent (Tricumed TM4, 20.7 mm) and a newly developed biomechanical valve (Engage aortic valve Model 6000, 21.0 mm). All valves including the human aortic valve were assessed by videotape observation under pulsatile flow conditions. Measured flow-related parameters include in vitro mean transvalvular pressure, regurgitant volume, effective orifice area and performance index. RESULTS: The optical assessment of all five valves demonstrated a complete opening during systole and closing at the beginning of diastole. All valves were optically sufficient during diastole. Engage aortic valve Model 6000 showed the highest maximum transvalvular pressure (27.5 +/- 8.2 mmHg), whereas both Hall-Kaster (17.9 +/- 1.5 mmHg) and St. Jude Medical (16.7 +/- 0.7 mmHg) had a lower gradient than the native aortic valve (24.0 +/- 0.2 mmHg) and Tricumed TM4 (21.8 +/- 3.8 mmHg). The maximum effective orifice area of St. Jude Medical amounted to 258.7 +/- 3.4 mm(2), followed by Tricumed TM4 with an area of 222.1 +/- 1.9 mm(2) and the human aortic valve with 160.4 +/- 2.9 mm(2). Hall-Kaster and Engage aortic valve Model 6000 had an area of 198.9 +/- 1.6 mm(2) and 176.7 +/- 3.1 mm(2), respectively. CONCLUSIONS: The pulse duplicator proved to be highly accurate and yielded reproducible results. Since it has been calibrated with a human aortic valve, the hemodynamics of any heart valve prosthesis can be compared with the human valve. This system can evaluate and promote the development of new biological and mechanical heart valve prostheses.