Ongoing Myocardial Damage Research Articles

6390 Takotsubo Cardiomyopathy (Case Report)

Abstract Disclosure: H.A. Ballout: None. I. Malas: None. Z. Sakor: None. M. Ismail: None. C. Najjar: None. Takotsubo is a reversible stress-induced cardiomyopathyusually associated with emotional or physical stress.Thyroid stormhas been identified as a rare cause of takotsubo. We report a rarecase of 64-year-old female presented with high BP. Blood testsshowed elevated troponin level and high FT4 FT4 Cardiacultrasound revealed normal size of the LV &anteroseptal wallakynisia,low ejection fraction,&diastolic LVD.Cardiac cathshowed normal coronary arteries, ventriculography showed apicalballooning and bulging in the left ventricle, suggesting Takotsubocardiomyopathy as a final diagnosis. patient was treated for thethyroid storm&takotsubo cardiomyopathy.month later she showedsignificant improvement in the cardiac function &thyroid hormone levels. As this case represented a rare stress-induced cardiomyopathy, the early diagnosis &suitable therapy areessential to prevent ongoing myocardial damage and providebetter chance for recovery. Presentation: 6/2/2024

Is heart-type fatty acid binding protein (H-FABP) a valid marker of arterial stiffness in patients with systemic sclerosis?

Background/Aim: Both micro- and macro-vascular involvement has been researched in systemic sclerosis (SSc) for many years. In this study, the relationship of arterial stiffness with heart-type fatty acid binding protein (h-FABP), which is well-accepted as a cardiac marker, was investigated for the first time.
 Methods: In this case-control study, 40 patients diagnosed with SSc between the ages of 18 and 65 were included. Thirty healthy individuals of similar age and gender were included as the control group. Patients were excluded from the study if they had cardiovascular risk factors, active infections, and/or malignancies. Along with detecting biochemical markers in the blood, results from methods, such as 24-h blood pressure Holter recordings, pulse-wave velocities (PWV), and echocardiograms (ECHO) were obtained from patients.
 Results: The homocysteine mean level was higher in the patient group than in the control group (P < 0.001). H-FABP and asymmetric dimethylarginine (ADMA) means were similar between the two groups (P = 0.286 and P = 0.340, respectively). Vascular parameters, including mean arterial pressure (MAP), augmentation index normalized to the 75 /min heart rate (AIx @ 75), and PWV were also similar between the two groups (P = 0.498, P = 0.382 and P = 0.180, respectively).
 Conclusion: It can be concluded that no ongoing myocardial damage occurs based on normotensive Holter findings, normal h-FABP levels, and ECHO findings in our patients. It is suggested that vasodilatory treatments, such as pentoxifylline and calcium channel blockers, which the patients receive for SSc treatment due to Raynaud Syndrome, may protect them from hypertension and therefore offer protection from myocardial damage.

Interleukin-6 is upregulated and may be associated with myocardial injury in some patients who have recovered from COVID-19.

Coronavirus disease (COVID-19) causes myocardial injury by inducing a cytokine storm in severe cases. Studies have reported that myocardial injury persists for a prolonged period during COVID-19 recovery, and cardiac troponin is a useful indicator of myocardial injury. The interleukin-6 (IL-6) level is known to be associated with the morbidity and mortality of COVID-19, but this association has not been studied during recovery. The current study examined the association between IL-6 levels and myocardial damage during COVID-19 recovery. Four of 209 patients (1.9%) who recovered from COVID-19 had elevated IL-6 levels. All 4 patients tested positive for high-sensitivity troponin T, and 3 patients had subclinical left ventricular (LV) dysfunction according to echocardiography. Positivity for IL-6 during COVID-19 recovery suggests ongoing myocardial damage due to inflammation.

Reperfusion Arrhythmia in Acute Myocardial Infarction: Clinical Implication and Management

Reperfusion is a critical component of myocardium survival in acute myocardial infarction to minimize infarct size and improve clinical prognosis. Reperfusion, on the other hand, may result in increased and accelerated myocardial injury, a condition known as reperfusion injury. Following reperfusion, several arrhythmias are observed, and it is called reperfusion arrhythmia. Reperfusion arrhythmia is one manifestation of reperfusion injury. Numerous modest studies have evaluated what reperfusion arrhythmias are defined. It is described as an arrhythmia that occurs immediately or within the first minutes after coronary blood flow is restored. Traditionally, Accelerated Idioventricular Rhythm (AIVR) has been seen as a reperfusion arrhythmia. However, reperfusion may reveal any arrhythmia (or none at all); conversely, AIVR may occur in the absence of reperfusion. Calcium excess within the cells is thought to be a significant factor in the development of reperfusion arrhythmias. This may affect the significant delay following depolarization and the regional heterogeneity of regional blood flow restoration inside the ischemic zone, resulting in reperfusion arrhythmia. In some studies, it was mentioned that these arrhythmias may be due to ongoing myocardial cell damage and ischemia. Arrhythmias associated with reperfusion require special attention since hemodynamics can deteriorate quickly. In this review, clinical significance and management of reperfusion arrhythmia, as well as its link with reperfusion injury will be discussed.

Myocardial Perfusion Reserve in Children with Friedreich Ataxia.

Children with Friedreich's ataxia (FA) are at risk of perioperative morbidity and mortality from severe unpredictable heart failure. There is currently no clear way of identifying patients at highest risk. We used myocardial perfusion reserve (MPR), an MRI technique used to assess the maximal myocardial blood flow above baseline, to help determine potential surgical risk in FA subjects. In total, seven children with genetically confirmed FA, ages 8-17years, underwent MPR stress testing using regadenoson. Six of the seven demonstrated impaired endocardial perfusion during coronary hyperemia. The same six were also found to have evidence of ongoing myocardial damage as illustrated by cardiac troponin I leak (range 0.04-0.17ng/mL, normal < 0.03ng/mL). None of the patients had a reduced ejection fraction (range 59-74%) or elevated insulin level (range 2.46-14.23mCU/mL). This retrospective study shows that children with FA develop MPR defects early in the disease process. It also suggests MPR may be a sensitive tool to evaluate underlying cardiac compromise and could be of use in directing surgical management decisions in children with FA.

The prognostic impact of the serum heart-type fatty acid-binding protein level in patients with sepsis who were admitted to the non-surgical intensive-care unit.

Ongoing myocardial damage at the acme of the sepsis status has not been sufficiently evaluated. The clinical data of 160 sepsis patients who require intensive care and 127 outpatients with chronic heart failure (HF) were compared as a retrospective cohort study. Thereafter, the sepsis patients were divided into 3 groups according to the serum heart-type fatty acid-binding protein (H-FABP) quartiles [low H-FABP = Q1 (n = 39), middle H-FABP = Q2/Q3 (n = 81), and high H-FABP = Q4 group (n = 40)]. The H-FABP level was measured within 15 min of admission. The serum H-FABP levels in the sepsis patients [26.6 (9.3-79.0) ng/ml] were significantly higher than in the choric HF patients [6.6 (4.6-9.7) ng/ml]. A Kaplan-Meier curve showed that the survival rate of the high-H-FABP group was significantly lower than that of the middle- and low-H-FABP groups. The multivariate Cox regression analysis for the 365-day mortality showed that the high-H-FABP group (hazard ratio: 6.544, 95% confidence interval [CI] 2.026-21.140; p = 0.002) was an independent predictor of the 365-day mortality. The same trend in the prognostic impact was significantly (p = 0.015) observed in the cohort that had not been suffering from the cardiac disease before admission. The serum H-FABP level was an independent predictor of the 365-day mortality in the patients who were emergently hospitalized in the intensive-care unit due to sepsis. Ongoing myocardial damage was detected in the majority of patients with sepsis, suggesting that ongoing myocardial damage might be a candidate predictor of adverse outcomes in sepsis patients.

FDG-PET Imaging of Doxorubicin-Induced Cardiotoxicity: a New Window on an Old Problem

The present review focus on the published literature about the use of 18F-fluorodeoxyglucose (FDG) PET/CT imaging in the early recognition of anthracyclines-related cardiotoxicity. The application of PET/CT may represent an early predictor of subsequent cardiotoxicity in cancer patients treated with doxorubicin (DXR). However, the application of PET/CT may also extend beyond mere cardiotoxicity identification and monitoring to provide mechanistic delineation of the cardiotoxic pathophysiology. Indeed, this tool further enriched the current knowledge on energy metabolism impairment in the DXR-induced cardiotoxic cascade. The capability of FDG to selectively track the early endoplasmic reticulum pentose phosphate pathway (PPP) response to oxidative stress rather than the later occurring contractile dysfunction might imply the abrupt occurrence of metabolic abnormality during the course of chemotherapy, possibly identifying the ongoing myocardial damage in time to change the chemotherapy scheme or to initiate targeted cardioprotective treatments. Future prospective studies encompassing a specific dietary or pharmacologic preparation before FDG injection, as already performed in infectious and inflammatory heart diseases, are needed to move the obtained preclinical findings supporting the role of FDG imaging in DXR cardiotoxicity from bench to bedside.

P1653Admission high-sensitivity troponin T and NT-proBNP for outcome prediction in acute heart failure

Abstract Background High-sensitivity troponin T (hs-TnT) reflects the severity of ongoing myocardial damage and holds independent prognostic significance in chronic heart failure (HF). In acute HF (AHF), its additive prognostic value over natriuretic peptides is unclear. Methods Individual data of 1571 AHF patients with admission hs-TnT were collected from 3 cohorts. Results Patients were aged 78±10 years, and 51% were men. Median hs-TnT and N-terminal fraction of pro-B-type natriuretic peptide (NT-proBNP) concentrations were 43 ng/L (interquartile interval 26–69) and 5660 (2693–12466), respectively. Patients experiencing in-hospital death (n=187, 13%) had significantly higher hs-TnT and NT-proBNP on admission (both p&lt;0.001). The risk of in-hospital death increased by 45% per each doubling of hs-TnT (HR 1.45, 95% confidence interval - CI 1.31–1.59, p&lt;0.001), and by 32% per each doubling of NT-proBNP (HR 1.32, 95% CI 1.17–1.50, p&lt;0.001). Patients with hs-TnT ≥43 ng/L and NT-proBNP ≥5660 ng/L had a 2.7-fold higher risk of in-hospital death (relative risk - RR 2.7, 95% CI 1.7–4.5). Among the 1262 patients discharged, 1024 deaths occurred over a median 11-month follow-up (4–22). In a model including NT-proBNP, hs-TnT ≥43 ng/L was a strong, independent predictor of all-cause death at 6, 12 and 24 months, and the composite of cardiovascular death or HF hospitalization at 6 and 24 months. hs-TnT ≥43 ng/L also improved risk reclassification. Conclusions The risk of in-hospital death is almost 3 folds higher with admission hs-TnT ≥43 ng/L and NT-proBNP ≥5660 ng/L, and hs-TnT ≥43 ng/L holds strong independent prognostic significance for post-discharge outcome.

Admission high-sensitivity troponin T and NT-proBNP for outcome prediction in acute heart failure

BackgroundHigh-sensitivity troponin T (hs-TnT) reflects the severity of ongoing myocardial damage. In acute heart failure (AHF), its additive prognostic value over B-type natriuretic peptides is unclear. MethodsIndividual data of 1499 AHF patients with admission hs-TnT were collected from 3 cohorts. ResultsPatients (78 ± 10 years, 51% men, N-terminal fragment of pro-B-type natriuretic peptide – NT-proBNP - 5660 [2693–12,466], hs-TnT 43 ng/L [26–69]) experiencing in-hospital death (n = 187, 13%) had significantly higher hs-TnT and NT-proBNP on admission (both p < 0.001). Patients with hs-TnT ≥43 ng/L and NT-proBNP ≥5660 ng/L had a 2.7-fold higher risk of in-hospital death (relative risk - RR 2.7, 95% confidence interval - CI 1.7–4.5). Among discharged patients, 1024 deaths (81%) occurred over 11 months (4–22). In the whole population, hs-TnT ≥43 ng/L predicted all-cause death at 6, 12 and 24 months independently from NT-proBNP ≥5660 ng/L.The best NT-proBNP cut-off for in-hospital mortality (4382 ng/L) independently predicted this endpoint, while the best hs-TnT cut-off (55 ng/L) did not. Patients with NT-proBNP ≥4382 ng/L and hs-TnT ≥55 ng/L had a 12-fold higher risk of in-hospital death (RR 11.7, 95% CI 6.9–19.7). The best hs-TnT cut-offs independently predicted all post-discharge outcomes. ConclusionsThe best NT-proBNP cut-off (4382 ng/L) independently predicts outcome, while the best hs-TnT (55 ng/L) does not; patients with both biomarkers ≥best cut-offs have a 12-fold higher risk of in-hospital mortality. Admission hs-TnT ≥43 ng/L and the best hs-TnT cut-offs hold independent prognostic significance for post-discharge outcome, while hs-TnT seems less predictive than NT-proBNP when considering absolute values.

Dynamics of high-sensitivity cardiac troponin T during therapy with balloon pulmonary angioplasty for chronic thromboembolic pulmonary hypertension.

AimsBalloon pulmonary angioplasty (BPA) is an interventional treatment modality for inoperable chronic thromboembolic pulmonary hypertension (CTEPH). Therapy monitoring, based on non-invasive biomarkers, is a clinical challenge. This post-hoc study aimed to assess dynamics of high-sensitivity cardiac troponin T (hs-cTnT) as a marker for myocardial damage and its relation to N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels as a marker for cardiac wall stress.Methods and resultsThis study included 51 consecutive patients who underwent BPA treatment and completed a 6-month follow-up (6-MFU) between 3/2014 and 3/2017. Biomarker measurement was performed consecutively prior to each BPA and at 6-MFU.In total, the 51 patients underwent an average of 5 BPA procedures. The 6-month survival rate was 96.1%. The baseline (BL) meanPAP (39.5±12.1mmHg) and PVR (515.8±219.2dyn×sec×cm-5) decreased significantly within the 6-MFU (meanPAP: 32.6±12.6mmHg, P<0.001; PVR: 396.9±182.6dyn×sec×cm-5, P<0.001). At BL, the median hs-cTnT level was 11 (IQR 6–16) ng/L and the median NT-proBNP level was 820 (IQR 153–1872) ng/L. The levels of both biomarkers decreased steadily after every BPA, showing the first significant difference after the first procedure. Within the 6-MFU, hs-cTnT levels (7 [IQR 5–12] ng/L; P<0.001) and NT-proBNP levels (159 [IQR 84–464] ng/l; P<0.001) continued to decrease. The hs-cTnT levels correlated with the PVR (rrs = 0.42; p = 0.005), the meanPAP (rrs = 0.32; p = 0.029) and the NT-proBNP (rrs = 0.51; p<0.001) levels at BL.ConclusionNon-invasive biomarker measurement provides valuable evidence for the decreasing impairment of myocardial function and structure during BPA therapy. Changes in hs-cTNT levels are suggestive for a reduction in ongoing myocardial damage.

Presence of Myocardial Damage Predicts Future Development of Hypertension in a Normotensive Japanese General Population: The Yamagata (Takahata) Study.

A modest rise in blood pressure (BP) reportedly increases cardiovascular mortality despite not reaching obvious hypertension, suggesting that target organ damages are latently induced by slight BP rising. The goal of this study was to determine whether presence of subclinical myocardial damage can predict the future development of hypertension in the normotensive general population. The cohort study was conducted with subjects who participated in a community-based annual health check. Normotensive subjects without prior cardiovascular diseases at baseline were eligible for analyses (n = 524, mean age 58 ± 9 years; 53% women). We measured heart-type fatty acid binding protein (H-FABP) at baseline as a biomarker of ongoing myocardial damage. Longitudinal changes in BP were examined during median follow-up period of 6.2 years, and we investigated the association between the baseline H-FABP level and longitudinal BP changes. During the follow-up, 177 subjects (34%) developed hypertension. In multivariate Cox proportional hazard analysis adjusted for potential confounders including age and baseline BP, presence of myocardial damage was significantly associated with the development of hypertension (hazard ratio 1.80, 95% confidence interval, 1.26-2.54; P = 0.0014). Furthermore, relative risk of myocardial damage for incident hypertension was higher in younger subjects and lower BP category. Presence of subclinical myocardial damage was independently associated with the future development of hypertension in the normotensive general population.

P28-5 - The Impact of Pulse Pressure on Silent and Ongoing Myocardial Damage in the General Population

Background: Pulse pressure (PP) is associated with increased afterload and myocardial oxygen demand. PP is also associated with poor prognosis in patients with myocardial infarction and heart failure with preserved ejection fraction. Silent myocardial damage is associated with cardiovascular mortality in the general population. The aim of this study was to investigate the relationship between PP and silent myocardial damage in the general population. Methods and Results: The present study included 3505 subjects who participated in health checkup. We measured serum heart-type fatty acid binding protein (H-FABP) and brain natriuretic peptide (BNP) levels as markers of silent myocardial damage. Subjects were divided into four groups according to the quartiles of PP. Subjects with the highest PP group showed higher serum H-FABP and BNP levels. Multivariate logistic analysis showed that the higher PP was independently associated with silent myocardial damage evaluated by H-FABP (odds ratio (OR): 1.12, P < .05) and BNP (OR: 1.10, P < .05). Receiver operating characteristic (ROC) analysis showed that PP performed best in predicting silent myocardial damage evaluated by H-FABP and BNP compared with systolic blood pressure (BP), diastolic BP, and mean BP (c-index regarding H-FABP: 0.61, P < .05; c-index regarding BNP: 0.61, P < .05). Conclusions: High PP was related to higher H-FABP and BNP levels, suggesting that asymptomatic subjects with high PP may be exposed to myocardial damage.

P4252Relationship between pulse pressure and silent and ongoing myocardial damage in the general population

P4252Relationship between pulse pressure and silent and ongoing myocardial damage in the general population

Gender-differences in the associations between circulating creatine kinase, blood pressure, body mass and non-alcoholic fatty liver disease in asymptomatic asians.

BackgroundCreatine kinase (CK) is a pivotal regulatory enzyme in energy metabolism linked to both blood pressure and cardio-metabolic components. However, data is lacking in a large population of asymptomatic Asians.Methods and resultsCardio-metabolic assessment including anthropometric measures and non-alcoholic fatty liver disease (NAFLD) were evaluated by abdominal echo in 4,562 consecutive subjects who underwent an annual health survey. Serum CK levels were related to blood pressure components [systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP)], anthropometric measures, and excessive adiposity in liver as indicated by NAFLD. Circulating CK levels ranged from 4 to 1842 IU/L (mean [SE]: 108.7 [1.1] IU/L) in the study population which consisted of 2522 males (mean age: 48.7 ± 11.2) and 2040 females (mean age: 49.4±11.5). In general, male subjects presented with higher circulating CK levels than females (mean ± SE: 127.3 ± 1.5 vs. 85.5 ± 1.3 IU/L, respectively, p < .001). Gender-differences in circulating CK levels were also observed with increasing age, which showed a more pronounced positive relationship with age in female subjects (gender interaction: p < .05). Furthermore, an elevated circulating CK level was independently associated with higher blood pressure, waist circumference and fat mass (FM), greater body mass index (BMI), increased lower estimated glomerular filtration rate (eGFR) and presence of NAFLD in multivariate analysis (all p < .05), with CK elevation more pronounced with greater BMI and FM in males compared with females (sex interaction: p < .05).ConclusionIn a large asymptomatic Asian population, circulating CK levels were increased with more advanced age, higher blood pressure, and greater body mass with gender differences. Our findings may be useful in interpreting elevated CK from subjects free of ongoing myocardial damage.

Combined assessment of myocardial damage and electrical disturbance in chronic heart failure.

AIMTo investigate feasibility of combined assessment of biochemical and electrophysiological myocardial impairment markers risk-stratifying patients with chronic heart failure (CHF).METHODSSerum levels of heart-type fatty acid binding protein (H-FABP) as a marker of ongoing myocardial damage and QRS duration on electrocardiogram were measured at admission in 322 consecutive patients with CHF. A prolonged QRS duration was defined as 120 ms or longer. The cut-off value for H-FABP level (4.5 ng/mL) was determined from a previous study. Patients were prospectively followed during a median follow up period of 534 d. The primary endpoint was cardiac deaths and rehospitalization for worsening CHF.RESULTSThere were 117 primary events, including 27 cardiac deaths and 90 rehospitalizations. Patients were stratified into four groups according to H-FABP level and QRS duration (≥ 120 ms). Multivariate analysis demonstrated that high H-FABP levels [hazard ratio (HR) = 1.745, P = 0.021] and QRS prolongation (HR 1.612, P = 0.0258) were independent predictors of cardiac events. Kaplan-Meier analysis demonstrated that the combination of high H-FABP levels and QRS prolongation could be used to reliably stratify patients at high risk for cardiac events (log rank test P < 0.0001).CONCLUSIONCombined assessment of myocardial damage and electrical disturbance can be used to risk-stratify patients with CHF.

Abstract 11686: Pericellular Amyloid Infiltration in Biopsy-proven Cardiac Amyloidosis

Background: Cardiac amyloidosis is a rare disease characterized by the myocardial infiltration of amyloid. There are several histopathological patterns of amyloid accumulation, of which pericellular amyloid pattern is classified when amyloid is observed around each cardiomyocyte in endomyocardial biopsy. However, the relationship between pericellular amyloid deposition pattern and clinical characteristics has not yet been investigated. Objective: We retrospectively investigated endomyocardial biopsy-proven cardiac amyloidosis with pericellular amyloid deposition. Methods: Thirty cardiac amyloidosis patients in our institution were included. Results: Thirteen patients (43%) were pathologically classified into pericellular amyloid deposition. In the baseline characteristics, the patients with pericellular deposition had significantly lower age (69 ± 9 vs. 75 ± 6 years, p = 0.032) and higher brain natriuretic peptide levels (681 ± 516 vs. 267 ± 393 pg/ml, p = 0.003), compared with those without pericellular deposition. Electrocardiographic findings revealed that patients with pericellular amyloid deposition had significantly higher incidence of low voltage (46 vs. 12%, p = 0.045) and pseudoinfarction pattern (46 vs. 6%, p = 0.015), compared with patients without pericellular deposition. Echocardiography revealed that patients with pericellular deposition had significantly decreased deceleration time (152 ± 49 vs. 191 ± 50 ms, p = 0.049). Hemodynamic findings did not show significant difference between groups. High-sensitivity cardiac troponin-T levels were also analyzed in 14 cardiac amyloidosis patients without ischemic heart disease. Patients with pericellular amyloid deposition had significantly higher high-sensitivity cardiac troponin-T levels, compared with patients without pericellular deposition (0.128 ± 0.07 vs. 0.046 ± 0.03 pg/ml, p = 0.016). Conclusion: Pericellular amyloid deposition pattern was associated with electrocardiographic abnormalities, diastolic dysfunction, and ongoing myocardial damage. Our data suggest direct amyloid infiltration around the cardiomyocytes may cause myocardial damage, providing possible pathophysiological implication of the failing heart in cardiac amyloidosis.

Comparison of the Effects of Levosimendan Dobutamine and Vasodilator Therapy on Ongoing Myocardial Injury in Acute Decompensated Heart Failure.

Cardiac troponins (cTn) are reliable and the most sensitive biomarker in the setting of acute decompensated heart failure (ADHF). Acute decompensated heart failure is usually associated with worsening chronic heart failure, and it may be caused by ongoing minor myocardial cell damage that may occur without any reported precipitating factors. We compared the short-term effect of levosimendan (LEV), dobutamine (DOB), and vasodilator treatment (nitroglycerin [NTG]) on myocardial injury with hemodynamic, neurohumoral, and inflammatory indicators. One hundred twenty-two patients with a mean age of 66 ± 9 years were treated with LEV (n = 40), DOB (n = 42), and NTG (n = 40) and examined retrospectively. Blood samples (cTnI, N-terminal probrain natriuretic peptide [NT-proBNP], highly sensitive C-reactive protein [HsCRP], and others), left ventricular ejection fraction (LVEF), systolic pulmonary artery pressure (sPAP), and 6-minute walk distance (6MWD) were compared before and after treatment. At admission, detectable levels of cTnI were observed in 53% of patients (≥0.05 ng/mL). Serial changes in the mean cTnI levels were not significantly different between the groups (LEV 0.04 ± 0.01 to 0.03 ± 0.01 ng/mL; DOB 0.145 ± 0.08 to 0.08 ± 0.03 ng/mL; NTG 0.1 ± 0.03 to 0.09 ± 0.02 ng/mL; overall P = .859). Favourable effects on the NT-proBNP, sPAP values, LVEF, 6MWD, and HsCRP were observed overall, especially in the LEV groups. Beneficial effects of short-term use of LEV, DOB, and NTG on ongoing myocardial injury were demonstrated. These findings can be attributed to the anti-ischemic properties as well as the hemodynamic, neurohumoral, and functional benefits from the positive inotropes, especially LEV, in patients with ADHF.

Balloon pulmonary angioplasty attenuates ongoing myocardial damage in patients with chronic thromboembolic pulmonary hypertension

Balloon pulmonary angioplasty attenuates ongoing myocardial damage in patients with chronic thromboembolic pulmonary hypertension

Abstract 13252: High-sensitivity Troponin T is a Useful Biomarker of Hemodynamics Response After Balloon Pulmonary Angioplasty in Patients With Chronic Thromboembolic Pulmonary Hypertension

Introduction: Balloon pulmonary angioplasty (BPA) improves hemodynamics in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Cardiac troponin is a marker of ongoing myocardial damage, and reflects hemodynamics in patients with left-heart failure. However, the clinical significance of cardiac troponin in CTEPH patients treated with BPA was unknown. We hypothesized that cardiac troponin is a surrogate marker of hemodynamic response in CTEPH patients who underwent BPA. Methods and Results: We analyzed 63 consecutive CTEPH patients who underwent BPA procedures, and measured high-sensitivity troponin T (hsTnT) level using electrochemiluminescence immunoassay before and after BPA from November 2012 to May 2015 (age; 62.8±14.3 years, female; n=41, number of target vessels per patient; 13.3±2.4, total sessions per patient; 5.9±1.9). Elevation of baseline hsTnT was associated with older age (p&lt;0.05). Patients with baseline hsTnT level &gt; median value (0.012 ng/ml) was associated with higher right atrium pressure (7.5±3.8 vs 5.9±2.2 mmHg, p&lt;0.05), mean pulmonary artery pressure (mPAP; 41.4±11.0 vs 34.9±9.6 mmHg, p&lt;0.05), pulmonary vascular resistance (PVR; 926.7±663.3 vs 731.1±931.8 dynes•sec•cm-5, p&lt;0.05) and lower pulmonary capillary wedge pressure (8.2±2.9 vs 10.4±4.9 mmHg, p&lt;0.05) and six-minute walk distance (265.9±98.9 vs 342.0±80.9 m, p&lt;0.05), but not associated with cardiac output. BPA improved mPAP (from 38.1±10.7 to 21.1±5.6 mmHg, p&lt;0.05) and PVR (from 823.6±828.2 to 292.8±129.6 dynes•sec•cm-5, p&lt;0.05). HsTnT significantly decreased after BPA (from 0.015±0.012 to 0.012±0.009 ng/mL; p&lt;0.05). Based on change of HsTnT after BPA, we divided the patients into two groups: HsTnT-decrease group (n=34) and HsTnT-increase or stable group (n=29). HsTnT-decrease group showed greater decreases in mPAP and PVR (delta mPAP 20.1±10.3 vs 13.3±11.3 mmHg, p&lt;0.05, delta PVR 686.4±982.6 vs 352.3±452.5 dynes•sec•cm-5, p&lt;0.05) after BPA. Conclusions: HsTnT level is a useful biomarker of hemodynamics severity, and change of hsTnT reflected improvement of hemodynamics in CTEPH patients who underwent BPA. Serial measurements of hsTnT could be a less-invasive and useful strategy to monitor therapeutic impact of BPA.

Abstract 13337: 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 for 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.