Pathophysiology of Advanced Heart Failure

Biegus, Jan; Niewiński, Piotr; Josiak, Krystian; Kulej, Katarzyna; Ponikowska, Barbara; Nowak, Krzysztof; Zymliński, Robert; Ponikowski, Piotr

doi:10.1016/j.hfc.2021.06.001

Cited by 12 publications

(6 citation statements)

References 84 publications

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“…In contrast to the earlier reports [ 25 ] suggesting that increased inflammatory response with subsequent increased production of inflammatory markers in patients with HF could potentially affect the coagulation cascade, induce an endothelial dysfunction, and hemodynamic imbalance [ 26 , 27 ] leading to decompensation of heart failure, thus increasing the rate of an unfavorable outcome [ 28 ], in our cohort study, no significant differences were observed regarding the levels of inflammatory markers on admission. A similar interesting observation was made for the non-HF cohort.…”

Section: Discussioncontrasting

confidence: 99%

Usefulness of C2HEST Score in Predicting Clinical Outcomes of COVID-19 in Heart Failure and Non-Heart-Failure Cohorts

Rola¹,

Doroszko

Trocha

et al. 2022

JCM

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Background: Patients with heart failure represent a vulnerable population for COVID-19 and are prone to having worse prognoses and higher fatality rates. Still, the clinical course of the infection is dynamic, and complication occurrence in particular in patients with heart failure is fairly unpredictable. Considering that individual components of the C2HEST (C2: Coronary Artery Diseases (CAD)/Chronic obstructive pulmonary disease (COPD); H: Hypertension; E: Elderly (Age ≥ 75); S: Systolic HF; T: Thyroid disease) are parallel to COVID-19 mortality risk factors, we evaluate the predictive value of C2HEST score in patients with heart failure (HF) Material and Methods: The retrospective medical data analysis of 2184 COVID-19 patients hospitalized in the University Hospital in Wroclaw between February 2020 and June 2021 was the basis of the study. The measured outcomes included: in-hospital mortality, 3-month and 6-month all-cause-mortality, non-fatal end of hospitalization, and adverse in-hospital clinical events. Results: The heart failure cohort consists of 255 patients, while 1929 patients were assigned to the non-HF cohort. The in-hospital, 3-month, and 6-month mortality rates were highest in the HF cohort high-risk C2HEST stratum, reaching 38.61%, 53.96%, and 65.36%, respectively. In the non-HF cohort, in-hospital, 3-month, and 6-month mortalities were also highest in the high-risk C2HEST stratum and came to 26.39%, 52.78%, and 65.0%, respectively. An additional point in the C2HEST score increased the total death intensity in 10% of HF subjects (HR 1.100, 95% CI 0.968–1.250 p = 0.143) while in the non-HF cohort, the same value increased by 62.3% (HR 1.623, 95% CI 1.518–1.734 p < 0.0001). Conclusions: The C2HEST score risk in the HF cohort failed to show discriminatory performance in terms of mortality and other clinical adverse outcomes during hospitalization. C2HEST score in the non-HF cohort showed significantly better performance in terms of predicting in-hospital and 6-month mortality and other non-fatal clinical outcomes such as cardiovascular events (myocardial injury, acute heart failure, myocardial infarction, cardiogenic shock), pneumonia, sepsis, and acute renal injury.

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Section: Discussioncontrasting

confidence: 99%

Usefulness of C2HEST Score in Predicting Clinical Outcomes of COVID-19 in Heart Failure and Non-Heart-Failure Cohorts

Rola¹,

Doroszko

Trocha

et al. 2022

JCM

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“…Therefore, the question remains to what extent these structural abnormalities are present in HFpEF patients at an earlier stage, and whether these abnormalities are a cause of advanced HF or a consequence. For example, reduction of cardiac output can impair organ perfusion and myocardial function through neurohumoral activation [100,101]. Two imaging studies provide indirect information on cardiac capillary rarefaction, although findings are not consistent and controls had considerably fewer comorbidities, including less diabetes mellitus.…”

Section: Capillary Rarefaction In Hfpefmentioning

confidence: 99%

The Role of Systemic Microvascular Dysfunction in Heart Failure with Preserved Ejection Fraction

et al. 2022

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Heart failure with preserved ejection fraction (HFpEF) is a condition with increasing incidence, leading to a health care problem of epidemic proportions for which no curative treatments exist. Consequently, an urge exists to better understand the pathophysiology of HFpEF. Accumulating evidence suggests a key pathophysiological role for coronary microvascular dysfunction (MVD), with an underlying mechanism of low-grade pro-inflammatory state caused by systemic comorbidities. The systemic entity of comorbidities and inflammation in HFpEF imply that patients develop HFpEF due to systemic mechanisms causing coronary MVD, or systemic MVD. The absence or presence of peripheral MVD in HFpEF would reflect HFpEF being predominantly a cardiac or a systemic disease. Here, we will review the current state of the art of cardiac and systemic microvascular dysfunction in HFpEF (Graphical Abstract), resulting in future perspectives on new diagnostic modalities and therapeutic strategies.

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“…It is essential to acknowledge that patients with low serum osmolarity, despite being relatively young, exhibited characteristics of more severe HF. These included: lower blood pressure and lower serum sodium concentration as well as: high NTproBNP, elevated bilirubin, and low albumin concomitant with the highest vasopressin concentration [ 24 , 25 ]. On the other hand, the high osmolarity group had a different profile.…”

Section: Discussionmentioning

confidence: 99%

Serum Osmolarity and Vasopressin Concentration in Acute Heart Failure—Influence on Clinical Course and Outcome

et al. 2022

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Neurohormone activation plays an important role in Acute Heart Failure (AHF) pathophysiology. Serum osmolarity can affect this activation causing vasopressin excretion. The role of serum osmolarity and vasopressin concentration and its interaction remain still unexplored in AHF. The objective of our study was to evaluate the relationship of serum osmolarity with clinical parameters, vasopressin concentration, in-hospital course, and outcomes in AHF patients. The study group consisted of 338 AHF patients (male (76.3%), mean age of 68 ± 13 years) with serum osmolarity calculated by the equation: 1.86 × sodium [mmol/L] + (glucose [mg/dL]/18) + (urea [mg/dL]/2.8) + 9 and divided into osmolarity quartiles marked as: low: <287 mOsm/L, intermediate low: 287–294 mOsm/L, intermediate high: 295–304 mOsm/L, and high: >304 mOsm/L. There was an increasing age gradient in the groups and patients differed in the occurrence of comorbidities and baseline clinical and laboratory parameters. Importantly, analysis revealed that vasopressin presented a linear correlation with osmolarity (r = −0.221, p = 0.003) and its concentration decreased with quartiles (61.6 [44.0–81.0] vs. 57.8 [50.0–77.3] vs. 52.7 [43.1–69.2] vs. 45.0 [30.7–60.7] pg/mL, respectively, p = 0.034). This association across quartiles was observed among de novo AHF (63.6 [55.3–94.5] vs. 58.0 [50.7–78.6] vs. 52.0 [46.0–58.0] vs. 38.0 [27.0–57.0] pg/mL, respectively, p = 0.022) and was not statistically significant in patients with acute decompensated heart failure (ADHF) (59.5 [37.4–80.0] vs. 52.0 [38.0–74.5] vs. 57.0 [38.0–79.0] vs. 50.0 [33.0–84.0] pg/mL, respectively, p = 0.849). The worsening of renal function episodes were more frequent in quartiles with higher osmolarity (4 vs. 2 vs. 13 vs. 11%, respectively, p = 0.018) and patients that belonged to the quartiles with low and high osmolarity were characterized more often by incidence of worsening heart failure (20 vs. 9 vs. 10 vs. 22%, respectively, p = 0.032). There was also a U-shape distribution in relation to one-year mortality (31 vs. 19 vs. 23 vs. 37%, respectively, p = 0.022). In conclusion, there was an association of serum osmolarity with clinical status and both in-hospital and out-of-hospital outcomes. Moreover, the linear dependence between vasopressin concentration and serum osmolarity in the AHF population was identified and was driven mainly by patients with de novo AHF which suggests different pathophysiological paths in ADHF and AHF de novo.

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Pathophysiology of Advanced Heart Failure

Cited by 12 publications

References 84 publications

Usefulness of C2HEST Score in Predicting Clinical Outcomes of COVID-19 in Heart Failure and Non-Heart-Failure Cohorts

Usefulness of C2HEST Score in Predicting Clinical Outcomes of COVID-19 in Heart Failure and Non-Heart-Failure Cohorts

The Role of Systemic Microvascular Dysfunction in Heart Failure with Preserved Ejection Fraction

Serum Osmolarity and Vasopressin Concentration in Acute Heart Failure—Influence on Clinical Course and Outcome

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