Lymphatic morphology and function in chronic right heart failure due to secondary tricuspid valve regurgitation.

BACKGROUND: In heart failure, the capacity of the lymphatic system dictates symptoms of circulatory congestion. This study aimed at describing structural and functional changes of the lymphatic system in patients with chronic right-sided heart failure. METHODS: Individuals with long-standing severe tricuspid valve regurgitation and symptoms of heart failure were compared with age- gender- and weight-matched controls. Lymphatic structure and function were examined using non-contrast MR lymphangiography and near-infrared fluorescence imaging. Microvascular fluid dynamics and distribution were evaluated using strain gauge plethysmography and bio-impedance. RESULTS: In total nine patients and nine controls were included. Lymphatic morphology was unchanged in cases compared to controls with similar thoracic duct diameters 3.1(2.1-3.5) mm vs. 2.0(1.8-2.4) mm (p-value = 0.11), similar lymphatic classifications (p-value 0.34), and an identical number of lymphatic vessels in the legs 6 ± 1 vs. 6 ± 3 vessels/field (p-value = 0.72). Lymphatic function was comparable with contraction frequencies of 0.5 ± 0.2 and 0.5 ± 0.3 /min (p-value = 0.52) and a maximal lymphatic pumping pressure of 60 ± 13 and 57 ± 12 mmHg (p-value = 0.59) for cases and controls respectively. Finally, microvascular capillary filtration, isovolumetric threshold, and fluid distribution were similar between groups (p-value≥0.16 for all comparisons). CONCLUSION: In this small exploratory study, individuals with severe secondary tricuspid valve regurgitation and right-sided heart failure displayed a largely similar lymphatic anatomy and function. Thoracic duct diameter displayed a trend towards increased size in the patient group. We speculate that cases were indeed stable and optimally treated at the time of examination, and with a lymphatic system largely unaffected by any of the current or prior hemodynamic changes.

[Trikuspidalklapinsufficiens].

Tricuspid regurgitation (TR) has in recent literature been described as an independently progressive disorder associated with a poor prognosis. Studies have emphasized the importance of a more proactive approach in treating TR in order to prevent progression of right ventricular dysfunction and ultimately right heart failure. These findings have renewed interest in surgical treatment for isolated TR whilst also fueling rapid advancements in transcatheter therapies, as argued in this review.

Clinical performance and exercise hemodynamics in patients with severe secondary tricuspid regurgitation and chronic atrial fibrillation.

OBJECTIVE: The study aimed to investigate the functional capacity and hemodynamics at rest and during exercise in patients with chronic atrial fibrillation and severe functional symptomatic tricuspid regurgitation (AF-FTR). BACKGROUND: Symptoms and clinical performance of severe AF-FTR mimic the population of patients with heart failure with preserved ejection fraction (HFpEF). Severe AF-FTR is known to be associated with an adverse prognosis whereas less is reported about the clinical performance including exercise capacity and hemodynamics in patients symptomatic AF-FTR. METHODS: Right heart catheterization (RHC) at rest and during exercise was conducted in a group of patients with stable chronic AF-TR and compared with a group of patients with HFpEF diagnosed with cardiac amyloid cardiomyopathy (CA). All patients had preserved ejection fraction and no significant left-sided disease. RESULTS: Patients with AF-FTR demonstrated a low exercise capacity that was comparable to CA patients (TR 4.9 ± 1.2 METS vs. CA 4. 7 ± 1.5 METS; P = 0.78) with an average peak maximal oxygen consumption of 15 mL/min/kg. Right atrium pressure increased significantly more in the AF-FTR patients as compared to CA patients at peak exercise (25 ± 8 vs 19 ± 9, p < 0.01) whereas PCWP increased significantly to a similar extent in both groups (31 ± 4 vs 31 ± 8 mmHg, p = 0.88). Cardiac output (CO) was significantly lower among AF-FTR at rest as compared to CA patients (3.6 ± 0.9 vs 4.4 ± 1.3 l/min; p < 0.05) whereas both groups demonstrated a poor but comparable CO reserve at peak exercise (7.3 ± 2.9 vs 7.9 ± 3.8 l/min, p = 0.59). CONCLUSIONS: AF-FTR contributes to the development of advanced heart failure symptoms and poor exercise capacity reflected in increased atrial filling pressures, reduced cardiac output at rest and during exercise sharing common features seen in HFpEF patients with other etiologies.

All-Cause Mortality and Cardiovascular Outcomes With Non-Vitamin K Oral Anticoagulants Versus Warfarin in Patients With Heart Failure in the Food and Drug Administration Adverse Event Reporting System.

BACKGROUND: Many patients with heart failure (HF) are treated with warfarin or non-vitamin K oral anticoagulants (NOACs). Randomized outcome-driven comparisons of different anticoagulant strategies in HF are lacking. Data from international, government-mandated registries may be useful in understanding the real-life use of various anticoagulants and how they are linked to outcomes. STUDY QUESTION: To assess 2015 annual all-cause mortality, myocardial infarction, and stroke rates co-reported for warfarin and NOACs in subjects with and without HF in the US Food and Drug Administration Adverse Event Reporting System (FAERS) database. STUDY DESIGN: We extracted and examined outcome cases in subjects with HF and on warfarin, dabigatran, rivaroxaban, apixaban, or edoxaban and stratified these according to anticoagulants. MEASURES AND OUTCOMES: Annual all-cause mortality, myocardial infarction, and stroke in FAERS. ANALYSIS METHOD: Odds ratio (OR) and χ(Equation is included in full-text article.)for oral anticoagulants from FAERS with and without HF among complete primary reports issued in 2015. RESULTS: FAERS reported 137,026 HF cases, with death co-reported in 42,942 (31.3%). In total, 11,278 (8.2%) HF patients were treated with anticoagulants, with more prescribed warfarin (n = 8260) than all NOACs combined (n = 3018). Very few reports for edoxaban were available. Warfarin consistently displayed a signal for excess adverse events compared to NOACs: OR (95% confidence interval) for the composite of mortality, myocardial infarction, and stroke were 1.91 (1.76-2.07) versus apixaban, 1.92 (1.81-2.03) versus dabigatran, 4.09 (3.38-4.37) versus rivaroxaban, and 2.64 (2.53-2.76) versus all NOACs combined (all P < 0.001). Warfarin, compared to all NOACs combined, demonstrated higher rates of all-cause mortality [OR = 2.69 (95% confidence interval, 2.49-2.90)], myocardial infarction [5.30 (4.17-6.74)], stroke [OR = 8.85 (6.61-11.84)], and ischemic stroke [OR = 12.73 (8.87-18.27); all P < 0.001]. CONCLUSIONS: Annual 2015 FAERS profiles in HF patients reveal that warfarin was numerically dominant. Warfarin was associated with higher risk of death, myocardial infarction, and stroke compared to NOACs. These observational data provide real-world insight into a potential safety benefit of NOACs over warfarin in the setting of HF.

B-type natriuretic peptides and mortality after stroke: a systematic review and meta-analysis.

OBJECTIVE: To measure the association of B-type natriuretic peptide (BNP) and N-terminal fragment of BNP (NT-proBNP) with all-cause mortality after stroke, and to evaluate the additional predictive value of BNP/NT-proBNP over clinical information. METHODS: Suitable studies for meta-analysis were found by searching MEDLINE and EMBASE databases until October 26, 2012. Weighted mean differences measured effect size; meta-regression and publication bias were assessed. Individual participant data were used to estimate effects by logistic regression and to evaluate BNP/NT-proBNP additional predictive value by area under the receiver operating characteristic curves, and integrated discrimination improvement and categorical net reclassification improvement indexes. RESULTS: Literature-based meta-analysis included 3,498 stroke patients from 16 studies and revealed that BNP/NT-proBNP levels were 255.78 pg/mL (95% confidence interval [CI] 105.10-406.47, p = 0.001) higher in patients who died; publication bias entailed the loss of this association. Individual participant data analysis comprised 2,258 stroke patients. After normalization of the data, patients in the highest quartile had double the risk of death after adjustment for clinical variables (NIH Stroke Scale score, age, sex) (odds ratio 2.30, 95% CI 1.32-4.01 for BNP; and odds ratio 2.63, 95% CI 1.75-3.94 for NT-proBNP). Only NT-proBNP showed a slight added value to clinical prognostic variables, increasing discrimination by 0.028 points (integrated discrimination improvement index; p < 0.001) and reclassifying 8.1% of patients into correct risk mortality categories (net reclassification improvement index; p = 0.003). Neither etiology nor time from onset to death affected the association of BNP/NT-proBNP with mortality. CONCLUSION: BNPs are associated with poststroke mortality independent of NIH Stroke Scale score, age, and sex. However, their translation to clinical practice seems difficult because BNP/NT-proBNP add only minor predictive value to clinical information.

Association of ischemic stroke to coronary artery disease using computed tomography coronary angiography.

BACKGROUND: While patients with coronary artery disease (CAD) and cerebrovascular disease share similar risk factor profiles, data on whether IS can be considered a "CAD equivalent" are limited. We aimed to determine whether ischemic stroke is an independent predictor of CAD by using cardiac computed tomography angiography (CTA). METHODS: We analyzed the CTA in 392 patients with no history of CAD (24 patients with acute IS and 368 patients with acute chest pain). Extent of plaque burden was additionally dichotomized into 0-4 versus >4 segments. RESULTS: Patients with IS had a near 5-fold increase odds of having coronary artery plaque (odds ratio [OR] 4.9, P<0.01) as compared to those without IS. After adjustment for age, gender, and traditional cardiac risk factors, there remained a near 4-fold increase odds for coronary plaque (adjusted OR 3.7, P=0.04). When stratified by extent of plaque, patients with IS had over 18-fold increase odds of having >4 segments of plaque than 0-4 segments as compared to patients without stroke (OR 18.3, P<0.01), which remained significantly associated in adjusted analysis (adjusted OR 12.1, P<0.001). CONCLUSION: Acute IS is independently associated with higher risk and greater extent of CAD compared to patients with acute chest pain at low-to-intermediate risk for acute coronary syndrome.

Fatty Acid binding protein 4 is associated with carotid atherosclerosis and outcome in patients with acute ischemic stroke.

BACKGROUND AND PURPOSE: Fatty acid binding protein 4 (FABP4) has been shown to play an important role in macrophage cholesterol trafficking and associated inflammation. To further elucidate the role of FABP4 in atherogenesis in humans, we examined the regulation of FABP4 in carotid atherosclerosis and ischemic stroke. METHODS: We examined plasma FABP4 levels in asymptomatic (n = 28) and symptomatic (n = 31) patients with carotid atherosclerosis, as well as in 202 subjects with acute ischemic stroke. In a subgroup of patients we also analysed the expression of FABP4 within the atherosclerotic lesion. In addition, we investigated the ability of different stimuli with relevance to atherosclerosis to regulate FABP4 expression in monocytes/macrophages. RESULTS: FABP4 levels were higher in patients with carotid atherosclerosis, both systemically and within the atherosclerotic lesion, with particular high mRNA levels in carotid plaques from patients with the most recent symptoms. Immunostaining of carotid plaques localized FABP4 to macrophages, while activated platelets and oxidized LDL were potent stimuli for FABP4 expression in monocytes/macrophages in vitro. When measured at the time of acute ischemic stroke, high plasma levels of FABP4 were significantly associated with total and cardiovascular mortality during follow-up, although we did not find that addition of FABP4 to the fully adjusted multivariate model had an effect on the prognostic discrimination for all-cause mortality as assessed by c-statistics. CONCLUSIONS: FABP4 is linked to atherogenesis, plaque instability and adverse outcome in patients with carotid atherosclerosis and acute ischemic stroke.

Activated leukocyte cell adhesion molecule and prognosis in acute ischemic stroke.

BACKGROUND AND PURPOSE: Biomarkers predicting mortality and functional outcome in stroke may be clinically helpful in identification of patients likely to benefit from intervention. Activated leukocyte cell adhesion molecule (ALCAM) is upregulated during neuroinflammation; we investigated whether ALCAM concentrations are associated with long-term mortality after ischemic stroke. METHODS: In 244 patients with acute ischemic stroke (age 69±13 years), samples of ALCAM were obtained serially from presentation to Day 5 and after 6 months. Patients with overt ischemic heart disease and atrial fibrillation were excluded. The patients were followed for 47 months with all-cause and cardiovascular mortality as end points. RESULTS: At follow-up, 72 patients (29%) had died, 43 due to cardiovascular causes. Patients with ALCAM in the fourth quartile (>46.8 ng/mL) at admission had a significantly poorer survival rate on univariate analysis (P<0.001); other time points did not add further but provided similar prognostic information. In multivariate analysis, after adjustment for age, stroke severity, C-reactive protein levels, troponin T levels, and heart and/or renal failure, ALCAM levels above the fourth quartile remained an independent predictor of long-term mortality (adjusted hazard ratio, 2.05; 95% CI, 1.11 to 3.76; P=0.021) and cardiovascular mortality (adjusted hazard ratio, 2.54; 95% CI, 1.06 to 6.07; P=0.028). CONCLUSIONS: ALCAM levels measured at admission of acute ischemic stroke are associated with long-term mortality.

Mitral valve perforation appearing years after radiofrequency ablation.

The case is reported of a young adult with Wolff-Parkinson-White (WPW) syndrome who, three years after a complicated radiofrequency (RF) catheter ablation procedure, developed dyspnea on exertion. Echocardiography revealed severe mitral valve regurgitation caused by a perforation of the posterior leaflet. Echocardiographic follow up is recommended after a complicated course of left-sided catheter ablation.

Early impact of prescription Omega-3 fatty acids on platelet biomarkers in patients with coronary artery disease and hypertriglyceridemia.

BACKGROUND: Prescription omega-3-acid ethyl esters (PO-3A) have been tested for outcome benefits in patients with coronary artery disease (CAD), arrhythmias and heart failure. Some evidence suggests that PO-3A may exert their benefit via inhibiting platelets. We tested the hypothesis that PO-3A may inhibit platelet activity in patients with documented stable CAD, beyond the antiplatelet properties of aspirin and statins. METHODS: Thirty patients with documented CAD and triglycerides over 250 mg/dl treated with aspirin (70-160 mg/daily) and statins (simvastatin equivalence dose: 5-40 mg/daily) were randomized 1:1:1 to Omacor™ 1 g/day (DHA/EPA ratio 1.25:1.0), Omacor 2 g/day, or a placebo for 2 weeks. Platelet tests including aggregometry and flow cytometry and cartridge analyzer readings were performed at baseline and at 1 and 2 weeks following PO-3A therapy. RESULTS: ADP-induced platelet aggregation (p = 0.037), GP IIb/IIIa antigen (p = 0.031) and activity (p = 0.024), and P-selectin (p = 0.041) were significantly reduced after PO-3A, while platelet/endothelial cell adhesion molecule (p = 0.09), vitronectin receptor (p = 0.16), formation of platelet-monocyte microparticles (p = 0.19) and the VerifyNow IIb/IIIa test (p = 0.27) only exhibited nonsignificant trends suggestive of reduced platelet activity. Finally, collagen- and arachidonic acid-induced aggregation, closure time with the PFA-100 device and expression of thrombospondin (CD36), GP Ib (CD42b), LAMP-3 (CD63), LAMP-1 (CD107a), CD40-ligand (CD154), GP37 (CD165), and PAR-1 receptor intact (SPAN 12) and cleaved (WEDE-15) epitopes were not affected by 2 weeks of PO-3A. CONCLUSION: Independently of the dose and already at 1 week, short-term therapy with PO-3A provided a modest reduction of platelet activity biomarkers, despite concomitant aspirin and statin therapy, when compared to a placebo. The effect of PO-3A is unique, differs from other known antiplatelet agents and suggests potential pleiotropism. These preliminary randomized data call for confirmation in prospective studies.

Relation of cardiac troponin I and microvascular obstruction following ST-elevation myocardial infarction.

BACKGROUND: Presence of microvascular obstruction (MVO) following primary percutaneous coronary intervention (pPCI) for ST-elevation myocardial infarction (STEMI) confers higher risk of left-ventricular remodelling and dysfunction. Measurement of cardiac troponin I (cTnI) after STEMI reflects the extent of myocardial destruction. We aimed to explore whether cTnI values were associated with presence of MVO independently of infarct size in STEMI patients receiving pPCI. METHODS: 175 patients with STEMI were included. cTnI was sampled at 24 and 48 h. MVO and infarct size was determined by delayed enhancement with cardiac magnetic resonance at five to seven days post index event. RESULTS: The presence of MVO following STEMI was associated with larger infarct size and higher values of cTnI at 24 and 48 h. For any given infarct size or cTnI value, there was a greater risk of MVO development in non-anterior infarctions. cTnI was strongly associated with MVO in both anterior and non-anterior infarctions (P < 0.01) after adjustment for covariates (including infarct size); and was reasonably effective in predicting MVO in individual patients (area-under-the-curve ≥0.81). CONCLUSION: Presence of MVO is reflected in levels of cTnI sampled at an early time-point following STEMI and this association persists after adjustment for infarct size.

Troponin I degradation in serum of patients with acute ischemic stroke.

BACKGROUND: Although troponin is a cornerstone biomarker in the assessment and management of patients with acute coronary syndrome, much remains to be learned about the biology of this widely used biomarker, including its post-release modification. Degradation of troponin following release in patients with acute coronary syndrome has been described; however whether such post-release modification occurs in other non-acute coronary syndrome states remains unknown. The aim of this study was to define troponin degradation in patients with acute ischemic stroke. MATERIALS AND METHODS: Troponin I (cTnI) was measured daily during the first 5 days of admission in 244 patients with acute ischemic stroke. Western blot analysis was performed using anti-cTnI antibodies and compared with serum concentrations of cTnI in seven patients and one patient with myocardial infarction (positive control). RESULTS: Elevated levels of troponin were detected in 25 (10%) patients; in all, both intact cTnI and cTnI degradation products were detected, with up to seven degradation fragments found. Samples with the highest total cTnI levels gave the strongest and most numerous western-blotting bands. All fragments were comparable with the degradation pattern of the positive control in terms of position. CONCLUSIONS: Immunoblotting of blood samples from patients with acute ischemic stroke reveals similar degradation patterns of cTnI as has been described in patients with acute myocardial infarction. The biological ramification and potential clinical impact of this finding bears further scrutiny.

Cardiac troponin I for the prediction of functional recovery and left ventricular remodelling following primary percutaneous coronary intervention for ST-elevation myocardial infarction.

OBJECTIVE: To investigate the ability of cardiac troponin I (cTnI) to predict functional recovery and left ventricular remodelling following primary percutaneous coronary intervention (pPCI) in ST-elevation myocardial infarction (STEMI). DESIGN: Post hoc study extending from randomised controlled trial. PATIENTS: 132 patients with STEMI receiving pPCI. MAIN OUTCOME MEASURES: Left ventricular ejection fraction (LVEF), end-diastolic and end-systolic volume index (EDVI and ESVI) and changes in these parameters from day 5 to 4 months after the index event. METHODS: Cardiac magnetic resonance examination performed at 5 days and 4 months for evaluation of LVEF, EDVI and ESVI. cTnI was sampled at 24 and 48 h. RESULTS: In linear regression models adjusted for early (5 days) assessment of LVEF, ESVI and EDVI, single-point cTnI at either 24 or 48 h were independent and strong predictors of changes in LVEF (p<0.01), EDVI (p<0.01) and ESVI (p<0.01) during the follow-up period. In a logistic regression analysis for prediction of an LVEF below 40% at 4 months, single-point cTnI significantly improved the prognostic strength of the model (area under the curve = 0.94, p<0.01) in comparison with the combination of clinical variables and LVEF at 5 days. CONCLUSION: Single-point sampling of cTnI after pPCI for STEMI provides important prognostic information on the time-dependent evolution of left ventricular function and volumes.

Comparison of usefulness of exercise testing versus coronary computed tomographic angiography for evaluation of patients suspected of having coronary artery disease.

In patients suspected of having coronary artery disease (CAD), we compared the diagnostic sensitivity and specificity of exercise testing using ST-segment changes alone and ST-segment changes, angina pectoris, and hemodynamic variables compared to coronary computed tomographic angiography (CTA). Quantitative invasive coronary angiography was the reference method (>50% coronary lumen reduction). A positive exercise test was defined as the development of significant ST-segment changes (> or =1 mV measured 80 ms from the J-point), and the occurrence of one or more of the following criteria: ST-segment changes > or =1 mV measured 80 ms from the J-point, angina pectoris, ventricular arrhythmia (the occurrence of > or =3 premature ventricular beats), and > or =20 mm Hg decrease in systolic blood pressure during the test. Positive results on CTA were defined as a coronary lumen reduction of > or =50%. In 100 patients (61 +/- 9 years old, 50% men, and 29% prevalence of significant CAD), the diagnostic sensitivity and specificity of exercise testing using ST-segment changes was 45% (95% confidence interval 53% to 87%) and 63% (95% confidence interval 61% to 84%), respectively. However, the inclusion of all test variables yielded a sensitivity of 72% (95% confidence interval 53% to 87%) and a specificity of 37% (95% confidence interval 26% to 49%). The diagnostic sensitivity of 97% (95% confidence interval 82% to 100%) and specificity of 80% (95% confidence interval 69% to 89%) for CTA, however, were superior to any of the exercise test analysis strategies. In conclusion, in patients suspected of having CAD, the diagnostic sensitivity of exercise testing significantly improves if all test variables are included compared to using ST-segment changes exclusively. Furthermore, the superior diagnostic performance of CTA for the detection and exclusion of significant CAD might favor CTA as the first-line diagnostic test in patients suspected of having CAD.

Usefulness of natriuretic peptide testing for long-term risk assessment following acute ischemic stroke.

Acute-phase levels of B-type natriuretic peptide (BNP) and the N-terminal fragment of the BNP prohormone (NT-pro-BNP) have been associated with mortality when measured in patients with an acute ischemic stroke; however, data regarding the longer-term value of NT-pro-BNP for long-term prognostication after ischemic stroke are limited. Two hundred sixteen patients (mean age 67 +/- 13 years) with acute ischemic stroke were seen 6 months after index admission at which time a structured evaluation including measurement of plasma NT-pro-BNP was performed. Patients were followed for 45 months, with all-cause mortality as the clinical end point. Median NT-pro-BNP concentration for the entire group was 147 pg/ml (10th to 90th percentiles 37 to 869). At follow-up 45 patients (21%) had died. NT-pro-BNP concentrations were significantly higher in decedents (308 pg/ml, 10th to 90th percentiles 74 to 2,279) than in the 171 survivors (132 pg/ml, 10th to 90th percentiles 35 to 570, p <0.001). Patients with NT-pro-BNP < or =147 pg/ml had a significantly improved survival rate on univariate analysis (p <0.001). In multivariate analysis after adjustment for age, stroke severity, heart and renal failures, levels of NT-pro-BNP were an independent predictor of mortality >6 months after stroke (adjusted hazard ratio 1.5, 95% confidence interval 1.1 to 1.9, p = 0.005). In conclusion, NT-pro-BNP concentrations measured during the stable phase after acute ischemic stroke are strongly predictive of long-term mortality.

Paradigm of pretest risk stratification before coronary computed tomography.

BACKGROUND: The optimal method of determining the pretest risk of coronary artery disease as a patient selection tool before coronary multidetector computed tomography (MDCT) is unknown. OBJECTIVE: We investigated the ability of 3 different clinical risk scores to predict the outcome of coronary MDCT. METHODS: This was a retrospective study of 551 patients consecutively referred for coronary MDCT on a suspicion of coronary artery disease. Diamond-Forrester, Duke, and Morise risk models were used to predict coronary artery stenosis (>50%) as assessed by coronary MDCT. The models were compared by receiver operating characteristic analysis. The distribution of low-, intermediate-, and high-risk persons, respectively, was established and compared for each of the 3 risk models. RESULTS: Overall, all risk prediction models performed equally well. However, the Duke risk model classified the low-risk patients more correctly than did the other models (P < 0.01). In patients without coronary artery calcification (CAC), the predictive value of the Duke risk model was superior to the other risk models (P < 0.05). Currently available risk prediction models seem to perform better in patients without CAC. Between the risk prediction models, there was a significant discrepancy in the distribution of patients at low, intermediate, or high risk (P < 0.01). CONCLUSIONS: The 3 risk prediction models perform equally well, although the Duke risk score may have advantages in subsets of patients. The choice of risk prediction model affects the referral pattern to MDCT.

Prevalence of electrocardiographic ST-T changes during acute ischemic stroke in patients without known ischemic heart disease.

We evaluated characteristics and prevalence of ST-segment depression and/or T-wave inversion in the resting electrocardiogram of 244 consecutive patients with acute ischemic stroke, but without ischemic heart disease. The prevalence of ST-T changes ranged from 13% to 16% and this is what to expect in the background population.

Evaluating the role of elevated levels of troponin in acute ischemic stroke.

Ischemic heart disease and cerebrovascular diseases may coexist in the same patient, and similar risk factors are shared. However, for several years, experimental and observational data have incessantly indicated that neurologically induced myocardial injury exists. This leaves the clinician with a diagnostic dilemma of how to distinguish between neurologically induced myocardial injury and myocardial infarction prior to the stroke. Since various alterations of the ECG have also been reported in this patient category, it has been suggested that elevated troponin levels are somehow neurologically mediated, thus not resulting from direct cardiac release. This review focuses on the available studies that systematically measured troponin in patients with acute ischemic stroke in order to properly interpret troponin elevations in these patients.