During the past few years, unexpected developments have driven studies in the field of clinical immunology. One driver of immense impact was the outbreak of a pandemic caused by the novel virus ...SARS-CoV-2. Excellent recent reviews address diverse aspects of immunological re-search into cardiovascular diseases. Here, we specifically focus on selected studies taking advantage of advanced state-of-the-art molecular genetic methods ranging from genome-wide epi/transcriptome mapping and variant scanning to optogenetics and chemogenetics. First, we discuss the emerging clinical relevance of advanced diagnostics for cardiovascular diseases, including those associated with COVID-19-with a focus on the role of inflammation in cardiomyopathies and arrhythmias. Second, we consider newly identified immunological interactions at organ and system levels which affect cardiovascular pathogenesis. Thus, studies into immune influences arising from the intestinal system are moving towards therapeutic exploitation. Further, powerful new research tools have enabled novel insight into brain-immune system interactions at unprecedented resolution. This latter line of investigation emphasizes the strength of influence of emotional stress-acting through defined brain regions-upon viral and cardiovascular disorders. Several challenges need to be overcome before the full impact of these far-reaching new findings will hit the clinical arena.
Background
Patients in heart transplantation (HTx) waiting list for advanced heart failure (HF) are susceptible to acute deterioration refractory to standard HF medical therapies. Limited data are ...available on long‐term in‐hospital continuous intravenous (IV) inotropic therapy as bridge to definite therapies.
Methods and results
We reviewed medical records of all heart transplant recipients treated in the pre‐HTx phase with in‐hospital continuous IV inotropes at our institution between 2012 and 2018. We analysed data before the beginning of continuous IV therapy and at the moment of HTx. We report data of 24 patients (mean age of 43.5 ± 15.7 years) treated with IV inotropes as bridge to HTx (median follow‐up of 28 months after HTx). The main length of IV inotropic therapy was 84 ± 66 days (min 22; max 264 days). At the beginning, the most frequently used inotrope was dopamine (median dosage of 3 mcg/kg/min, interquartile range 2.5–3.75), alone (n = 11, 46%) or in combination with other inotropes (n = 13, 54%). In 18 patients, the class of inotropes was changed during the hospitalization. We registered a progressive improvement of perfusion markers and neuro‐hormonal activation.
Conclusion
In‐hospital continuous parenteral inotropic therapy may serve as a temporary pharmacological bridge to HTx in patients with advanced HF that are actively listed to HTx with good reply in terms of prognosis and perfusion markers.
Abstract Background Although the prognostic value of right ventricular dysfunction in chronic heart failure (HF) has been studied extensively, it remains insufficiently characterized in the setting ...of acute decompensated HF (ADHF). We sought to assess whether measurement of tricuspid annular plane systolic excursion (TAPSE) or TAPSE-to–estimated pulmonary arterial systolic pressure (ePASP) ratio allows improvement of risk prediction in ADHF. Methods Four hundred ninety-nine patients with ADHF were studied. Cox regression analyses were used to analyze the association of TAPSE and TAPSE-to-ePASP ratio with 1-year mortality and logistic regression analyses to analyze the association of the 2 variables of interest with adverse in-hospital outcome (AiHO) (in-hospital death plus worsening HF). Results During the 365-day follow-up, 143 patients (28.7%) died. At univariable analysis, both TAPSE ( P = 0.026) and TAPSE-to-ePASP ratio ( P < 0.0001) were significantly associated with 1-year mortality. At multivariable Cox analysis, age ( P = 0.0270), ischemic heart disease ( P = 0.020), systolic blood pressure ( P = 0.006), log N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels ( P < 0.0001), serum sodium levels ( P = 0.001), and hemoglobin levels ( P = 0.001) at admission were independently associated with 1-year mortality. Adjusting for these covariates, neither TAPSE ( P = 0.314) nor TAPSE-to-ePASP ratio ( P = 0.237) remained independently associated with 1-year mortality. Eighty-three patients (16.6%) had an AiHO. At multivariable logistic regression analysis, the TAPSE-to-ePASP ratio was independently associated with an AiHO ( P = 0.024). The association of TAPSE alone or ePASP alone was not statistically significant. Conclusions Our data strongly suggest that early assessment of TAPSE or TAPSE-to-ePASP ratio does not improve prediction of 1-year mortality over other key risk markers in ADHF. Nonetheless, the TAPSE-to-ePASP ratio did appear to be independently associated with AiHO.
Background There has been significant controversy about the effects of pre‐hospitalization use of renin‐angiotensin system (RAS) inhibitors on the prognosis of patients with hypertension and ...coronavirus disease 2019. Methods and Results We retrospectively assessed 2297 hospitalized patients with coronavirus disease 2019 at Tongji Hospital in Wuhan, China, from January 10 to March 30, 2020; and identified 1182 patients with known hypertension on pre‐hospitalization therapy. We compared the baseline characteristics and in‐hospital mortality between patients with hypertension taking RAS inhibitors (n=355) versus non‐RAS inhibitors (n=827). Of the 1182 patients with hypertension (median age 68 years, 49.1% male), 12/355 (3.4%) patients died in the RAS inhibitors group versus 95/827 (11.5%) patients in the non‐RAS inhibitors group ( P <0.0001). Adjusted hazard ratio for mortality was 0.28 (95% CI 0.15–0.52, P <0.0001) at 45 days in the RAS inhibitors group compared with non‐RAS inhibitors group. Similar findings were observed when patients taking angiotensin receptor blockers (n=289) or angiotensin‐converting enzyme inhibitors (n=66) were separately compared with non‐RAS inhibitors group. The RAS inhibitors group compared with non‐RAS inhibitors group had lower levels of C‐reactive protein (median 13.5 versus 24.4 pg/mL; P =0.007) and interleukin‐6 (median 6.0 versus 8.5 pg/mL; P =0.026) on admission. The protective effect of RAS inhibitors on mortality was confirmed in a meta‐analysis of published data when our data were added to previous studies (odd ratio 0.44, 95% CI 0.29–0.65, P <0.0001). Conclusions In a large single center retrospective analysis, we observed a protective effect of pre‐hospitalization use of RAS inhibitors on mortality in patients with hypertension and coronavirus disease 2019, which might be associated with reduced inflammatory response.
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