Influenza A(H1N1) infection and severe cardiac dysfunction in adults: A case series

Zusammenfassung: HINTERGRUND: Während die virale Myokarditis und das Herzversagen anerkannte und gefürchtete Komplikationen einer saisonalen Influenza A Infektion sind, liegen bislang nur wenig Informationen über ein durch das 2009 Influenza A(H1N1) Virus induziertes Herzversagen vor. METHODEN UND HAUPTERGEBNISSE: Diese Fallsammlung fasst den Krankheitsverlauf von vier Patienten mit 2009 Influenza A(H1N1) Infektion zusammen, welche an unserer Klinik im Zeitraum von November 2009 bis September 2010 behandelt wurden. Alle Patienten präsentierten sich mit einer schweren kardialen Funktionsstörung (akutes Herzversagen, kardiogener Schock oder Herzkreislaufstillstand im Rahmen eines Kammerflimmerns) als das führende Symptom einer Influenza A(H1N1) Infektion. Zwei Patienten waren mit hoher Wahrscheinlichkeit kardial vorerkrankt, und drei benötigten eine Katecholamintherapie, um die hämodynamische Funktion zu stabilisieren. Mit Ausnahme eines Patienten der vor der Diagnosestellung der Influenza A(H1N1) Infektion verstarb, wurden alle Patienten mit einer antiviralen Therapie mit Oseltamivir und supportiver Intensivtherapie behandelt. Ein Acute Respiratory Distress Syndrom infolge der Influenza A(H1N1) Infektion trat bei einem Patienten auf. Die Herzfunktion normalisierte sich bei zwei Patienten und war bei einem Patienten noch bei Krankenhausentlassung eingeschränkt. SCHLUSSFOLGERUNG: Eine Influenza A(H1N1) Infektion kann mit einer schweren kardialen Funktionseinschränkung assoziiert sein. Diese kann sich sogar als führendes klinisches Symptom darstellen. Während einer Influenza Pandemie kann eine genaue Anamneseerhebung Grippeähnliche Symptome hervorbringen und sollte auch bei kritisch kranken Patienten mit akutem Herzversagen eine Diagnostik auf H1N1 Infektion veranlasse

Influenza A(H1N1) infection and severe cardiac dysfunction in adults: A case series

BACKGROUND: While viral myocarditis and heart failure are recognized and feared complications of seasonal influenza A infection, only limited information is available for 2009 influenza A(H1N1)-induced heart failure. METHODS AND MAIN FINDINGS: This case series summarizes the disease course of four patients with 2009 influenza A(H1N1) infection who were treated at our institution from November 2009 until September 2010. All patients presented with severe cardiac dysfunction (acute heart failure, cardiogenic shock or cardiac arrest due to ventricular fibrillation) as the leading symptom of influenza A(H1N1) infection. Two patients most likely had pre-existent cardiac pathologies, and three required catecholamine therapy to maintain hemodynamic function. Except for one patient who died before influenza A(H1N1) infection had been diagnosed, all patients received antiviral therapy with oseltamivir and supportive critical care. Acute respiratory distress syndrome due to influenza A(H1N1) infection developed in one patient. Heart function normalized in two of the three surviving patients but remained impaired in the other one at hospital discharge. CONCLUSIONS: Influenza A(H1N1) infection may be associated with severe cardiac dysfunction which can even be the leading clinical symptom at presentation. During an influenza pandemic, a thorough history may reveal flu-like symptoms and should indicate testing for H1N1 infection also in critically ill patients with acute heart failure

Effect of PEEP, blood volume, and inspiratory hold maneuvers on venous return

According to Guyton's model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to venous return (RVR) determine venous return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the impact of positive end expiratory pressure (PEEP) and blood volume on venous return and MSFP in pigs. MSFPRAO was measured by balloon occlusion of right atrium and MSFPinsp_hold extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, mean (SD) 12.9 (2.5) mmHg; PEEP 10 14.0 (2.6) mmHg, p=.002] without change in QPA [2.75 (.43) vs. 2.56 (.45) L/min, p=.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (2.2) and 16.4 (3.0) mmHg respectively p<.001], with parallel changes in QPA. Neither PEEP nor volume state altered RVR (p=.489). MSFPinsp_hold overestimated MSFPRAO [16.5 (5.8) mmHg vs.13.6 (3.2) mmHg; p=.001; mean difference 3.0 (5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightwards in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36 % (24 %) of pre-inspiratory hold at 15 cmH2O inspiratory pressure] and the QIVC recovery most complete at lowest inspiratory pressures independent of volume state [range from 80 (7) % after bleeding to 103 (8) % at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends venous return, possibly via hepatosplanchnic vascular waterfall

Preprocedural High-Sensitivity Cardiac Troponin T and Clinical Outcomes in Patients With Stable Coronary Artery Disease Undergoing Elective Percutaneous Coronary Intervention.

BACKGROUND Cardiac troponin detected by new-generation, highly sensitive assays predicts clinical outcomes among patients with stable coronary artery disease (SCAD) treated medically. The prognostic value of baseline high-sensitivity cardiac troponin T (hs-cTnT) elevation in SCAD patients undergoing elective percutaneous coronary interventions is not well established. This study assessed the association of preprocedural levels of hs-cTnT with 1-year clinical outcomes among SCAD patients undergoing percutaneous coronary intervention. METHODS AND RESULTS Between 2010 and 2014, 6974 consecutive patients were prospectively enrolled in the Bern Percutaneous Coronary Interventions Registry. Among patients with SCAD (n=2029), 527 (26%) had elevated preprocedural hs-cTnT above the upper reference limit of 14 ng/L. The primary end point, mortality within 1 year, occurred in 20 patients (1.4%) with normal hs-cTnT versus 39 patients (7.7%) with elevated baseline hs-cTnT (P<0.001). Patients with elevated hs-cTnT had increased risks of all-cause (hazard ratio 5.73; 95% confidence intervals 3.34-9.83; P<0.001) and cardiac mortality (hazard ratio 4.68; 95% confidence interval 2.12-10.31; P<0.001). Preprocedural hs-TnT elevation remained an independent predictor of 1-year mortality after adjustment for relevant risk factors, including age, sex, and renal failure (adjusted hazard ratio 2.08; 95% confidence interval 1.10-3.92; P=0.024). A graded mortality risk was observed across higher tertiles of elevated preprocedural hs-cTnT, but not among patients with hs-cTnT below the upper reference limit. CONCLUSIONS Preprocedural elevation of hs-cTnT is observed in one fourth of SCAD patients undergoing elective percutaneous coronary intervention. Increased levels of preprocedural hs-cTnT are proportionally related to the risk of death and emerged as independent predictors of all-cause mortality within 1 year. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT02241291