Quantifying Hemodynamic Cardiac Stress and Cardiomyocyte Injury in Normotensive and Hypertensive Acute Heart Failure.

BACKGROUND: The characterization of the different pathophysiological mechanisms involved in normotensive versus hypertensive acute heart failure (AHF) might help to develop individualized treatments. METHODS: The extent of hemodynamic cardiac stress and cardiomyocyte injury was quantified by measuring the B-type natriuretic peptide (BNP), N-terminal proBNP (NT-proBNP), and high-sensitivity cardiac troponin T (hs-cTnT) concentrations in 1152 patients presenting with centrally adjudicated AHF to the emergency department (ED) (derivation cohort). AHF was classified as normotensive with a systolic blood pressure (SBP) of 90-140 mmHg and hypertensive with SBP > 140 mmHg at presentation to the ED. Findings were externally validated in an independent AHF cohort (n = 324). RESULTS: In the derivation cohort, with a median age of 79 years, 43% being women, 667 (58%) patients had normotensive and 485 (42%) patients hypertensive AHF. Hemodynamic cardiac stress, as quantified by the BNP and NT-proBNP, was significantly higher in normotensive as compared to hypertensive AHF [1105 (611-1956) versus 827 (448-1419) pg/mL, and 5890 (2959-12,162) versus 4068 (1986-8118) pg/mL, both p < 0.001, respectively]. Similarly, the extent of cardiomyocyte injury, as quantified by hs-cTnT, was significantly higher in normotensive AHF as compared to hypertensive AHF [41 (24-71) versus 33 (19-59) ng/L, p < 0.001]. A total of 313 (28%) patients died during 360 days of follow-up. All-cause mortality was higher in patients with normotensive AHF vs. patients with hypertensive AHF (hazard ratio 1.66, 95%CI 1.31-2.10; p < 0.001). Normotensive patients with a high BNP, NT-proBNP, or hs-cTnT had the highest mortality. The findings were confirmed in the validation cohort. CONCLUSION: Biomarker profiling revealed a higher extent of hemodynamic stress and cardiomyocyte injury in patients with normotensive versus hypertensive AHF.

Pilot analysis of the usefulness of mortality risk score systems at resuscitated patients / Halálozásikockázat-becslo pontrendszerek alkalmazhatóságának elozetes vizsgálata újraélesztett betegek körében.

Összefoglaló. Bevezetés: A cardiovascularis halálokok közül világszerte nagy jelentoségu a hirtelen szívhalál. Annak ellenére, hogy a cardiopulmonalis resuscitatio és a postresuscitatiós intenzív osztályos kezelés is komoly metodikai és technikai fejlodésen ment keresztül az elmúlt idoszakban, kevés az olyan validált pontrendszer, amely jól becsülné a beteg intenzív osztályra kerülésekor a mortalitási rizikót. Célkituzés: A sikeres újraélesztést követo intenzív osztályos kezelés kezdetekor felmért, a cardiogen shock rizikóstratifikációjára alkalmazott CardShock Risk Score (CSRS) és az általunk hozzáadott, specifikus súlyozófaktorokkal (iniciális ritmus, inotropigény) módosított CardShock Risk Score (mCSRS) összevetése a mortalitás elorejelzésében post-cardiac arrest szindrómás betegeknél. Módszerek: Retrospektív vizsgálatunk során 172, kórházon kívül sikeresen újraélesztett és klinikánkon ellátott consecutiv betegbol a CSRS- és mCSRS-pontrendszerek segítségével végül 123 beteg adatait elemeztük. A CSRS- és mCSRS-változók és a korai/késoi mortalitás közötti összefüggést Cox-regressziós analízissel vizsgáltuk. A pontszámok alapján 3 csoportba (1-3, 4-6, 7+) soroltuk a betegeket. Az összevont csoportok túlélését log-rank teszttel hasonlítottuk össze. Eredmények: A betegpopuláció átlagéletkora 63,6 év volt (69% férfi), és a hirtelen szívhalál hátterében 80%-ban akut coronaria szindróma állt. A korai/késoi mortalitást leginkább a felvétel utáni neurológiai állapot, a szérumlaktátszint, a vesefunkció, az iniciális ritmus és a beteg katecholaminigénye határozta meg. A mCSRS alkalmazását követoen mind az "1-3" és a "4-6" (p≤0,001), mind a "4-6" és a "7+" (p = 0,006) csoportok között szignifikáns különbséget találtunk a túlélésben. Következtetés: A felvételkori pontok alapján a mCSRS pontosabban definiálja és differenciálja egymástól az általunk beválasztott két extra súlyozófaktorral az enyhe, a közepes és a magas mortalitási rizikóval bíró betegpopulációkat, mint a CSRS. Orv Hetil. 2021; 162(2): 52-60. INTRODUCTION: Sudden cardiac death is one of the most significant cardiovascular causes of death worldwide. Although there have been immense methodological and technical advances in the field of cardiopulmonary resuscitation and following intensive care in the last decade, currently there are only a few validated risk-stratification scoring systems for the quick and reliable estimation of the mortality risk of these patients at the time of admission to the intensive care unit. OBJECTIVE: Our aim was to correlate the mortality prediction risk points calculated by CardShock Risk Score (CSRS) and modified (m) CSRS based on the admission data of the post-cardiac arrest syndrome (PCAS) patients. METHODS: The medical records of 172 out-of-hospital resuscitated cardiac arrest patients, who were admitted at the Heart and Vascular Centre of Semmelweis University, were screened retrospectively. Out of the 172 selected patients, 123 were eligible for inclusion to calculate CSRS and mCSRS. Based on CSRS score, we generated three different groups of patients, with scores 1 to 3, 4 to 6, and 7+, respectively. Mortality data of the groups were compared by log-rank test. RESULTS: Mean age of the patients was 63.6 years (69% male), the cause of sudden cardiac death was acut coronary syndrome in 80% of the cases. The early and late mortality was predicted by neurological status, serum lactate level, renal function, initial rhythm, and the need of catecholamines. Using mCSRS, a significant survival difference was proven in between the groups "1-3" vs "4-6" (p≤0.001), "4-6" vs "7+" (p = 0.006). CONCLUSION: Compared to the CSRS, the mCSRS expanded with the 2 additional weighting points differentiates more specifically the low-moderate and high survival groups in the PCAS patient population treated in our institute. Orv Hetil. 2021; 162(2): 52-60.

Serum Lactate and A Relative Change in Lactate as Predictors of Mortality in Patients With Cardiogenic Shock - Results from the Cardshock Study.

INTRODUCTION: Cardiogenic shock complicating acute myocardial infarction has a very high mortality. Our present study focuses on serial measurement of lactate during admission due to cardiogenic shock and the prognostic effect of lactate and a relative change in lactate in patients after admission and the institution of intensive care treatment. METHODS AND RESULTS: This is a secondary analysis of the CardShock study. Data on lactate at baseline were available on 217 of 219 patients.In the study population, the median baseline lactate was 2.8 mmol/L (min-max range, 0.5-23.1 mmol/L).At admission, lactate was predictive of 30-day mortality with an adjusted Hazard ratio (HR) of 1.20 mmol/L (95% confidence interval, CI 1.14-1.27). Within the first 24 h of admission, baseline lactate remained predictive of 30-day mortality. Lactate at 6 h had a HR of 1.14 (95% CI 1.06-1.24) and corresponding values at 12 and 24 h had a HR of 1.10 (1.04-1.17), and of HR 1.19 (95% CI 1.07-1.32), respectively. A 50% reduction in lactate within 6 h resulted in a HR of 0.82 (95% CI 0.72-0.94). Corresponding hazard ratios at 12 and 24 h, were 0.87 (95% CI 0.76-0.98) and 0.74 (95% CI 0.60-0.91), respectively. CONCLUSION: The main findings of the present study are that baseline lactate is a powerful predictor of 30-day mortality, lactate at 6, 12, and 24 h after admission are predictors of 30-day mortality, and a relative change in lactate is a significant predictor of survival within the first 24 h after instituting intensive care treatment adding information beyond the information from baseline values.

Quantifying cardiac hemodynamic stress and cardiomyocyte damage in ischemic and nonischemic acute heart failure.

BACKGROUND: The early and noninvasive differentiation of ischemic and nonischemic acute heart failure (AHF) in the emergency department (ED) is an unmet clinical need. METHODS AND RESULTS: We quantified cardiac hemodynamic stress using B-type natriuretic peptide (BNP) and cardiomyocyte damage using 2 different cardiac troponin assays in 718 consecutive patients presenting to the ED with AHF (derivation cohort). The diagnosis of ischemic AHF was adjudicated using all information, including coronary angiography. Findings were validated in a second independent multicenter cohort (326 AHF patients). Among the 718 patients, 400 (56%) were adjudicated to have ischemic AHF. BNP levels were significantly higher in ischemic compared with nonischemic AHF (1097 [604-1525] pg/mL versus 800 [427-1317] pg/mL; P<0.001). Cardiac troponin T (cTnT) and sensitive cardiac troponin I (s-cTnI) were also significantly higher in ischemic compared with nonischemic AHF patients (0.040 [0.010-0.306] µg/L versus 0.018 [0.010-0.060] µg/L [P<0.001]; 0.024 [0.008-0.106] µg/L versus 0.016 [0.004-0.044 ] µg/L [P=0.002]). The diagnostic accuracy of BNP, cTnT, and s-cTnI for the diagnosis of ischemic AHF, as quantified by the area under the receiver-operating characteristic curve, was low (0.58 [95% CI, 0.54-0.63], 0.61 [95% CI, 0.57-0.66], and 0.59 [95% CI,0.54-0.65], respectively). These findings were confirmed in the validation cohort. CONCLUSIONS: At presentation to the ED, patients with ischemic AHF exhibit more extensive hemodynamic cardiac stress and cardiomyocyte damage than patients with nonischemic AHF. However, the overlap is substantial, resulting in poor diagnostic accuracy.