Abstract

BackgroundHantavirus infections cause potentially life-threatening disease in humans world-wide. Infections with American hantaviruses may lead to hantavirus pulmonary syndrome characterised by severe cardiopulmonary distress with high mortality. Pulmonary involvement in European Puumala hantavirus (PUUV) infection has been reported, whereas knowledge of potential cardiac manifestations is limited. We aimed to comprehensively investigate cardiopulmonary involvement in patients with PUUV-infection.MethodsTwenty-seven hospitalised patients with PUUV-infection were examined with lung function tests, chest high-resolution CT (HRCT), echocardiography including speckle tracking strain rate analysis, ECG and measurements of cardiac biomarkers N-terminal pro-B-type natriuretic peptide (NT-ProBNP) and troponin T. Patients were re-evaluated after 3 months. Twenty-five age and sex-matched volunteers acted as controls for echocardiography data.ResultsTwo-thirds of the patients experienced respiratory symptoms as dry cough or dyspnoea. Gas diffusing capacity was impaired in most patients, significantly improving at follow-up but still subnormal in 38%. HRCT showed thoracic effusions or pulmonary oedema in 46% of the patients. Compared to controls, the main echocardiographic findings in patients during the acute phase were significantly higher pulmonary vascular resistance, higher systolic pulmonary artery pressure, lower left ventricular ejection fraction and impaired left atrial myocardial motion. Pathological ECG, atrial fibrillation or T-wave changes, was demonstrated in 26% of patients. NT-ProBNP concentrations were markedly increased and were inversely associated with gas diffusing capacity but positively correlated to pulmonary vascular resistance. Furthermore, patients experiencing impaired general condition at follow-up had significantly lower gas diffusing capacity and higher pulmonary vascular resistance, compared to those feeling fully recovered.ConclusionsIn a majority of patients with PUUV-infection, both cardiac and pulmonary involvement was demonstrated with implications on patients’ recovery. The results demonstrate vascular leakage in the lungs that most likely is responsible for impaired gas diffusing capacity and increased pulmonary vascular resistance with secondary pulmonary hypertension and right heart distress. Interestingly, NT-ProBNP was markedly elevated even in the absence of overt ventricular heart failure. The method of simultaneous investigations of important cardiac and respiratory measurements improves the interpretation of the underlying pathophysiologic mechanisms.

Highlights

  • Hantavirus infections cause potentially life-threatening disease in humans world-wide

  • Pulmonary involvement is very common in Puumala hantavirus (PUUV)-infection, ranging from mild symptoms to severe lethal forms similar to hantavirus pulmonary syndrome (HPS) [8,9,10,11,12]

  • Previous studies of patients with HPS and PUUVrelated haemorrhagic fever with renal syndrome (HFRS) have shown impaired lung function, pleural effusion and pulmonary oedema [4,5,6,9,13,14], along with an activated lower airway immune response reported in both syndromes [11,12,15,16,17]

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Summary

Introduction

Hantavirus infections cause potentially life-threatening disease in humans world-wide. Infections with American hantaviruses may lead to hantavirus pulmonary syndrome characterised by severe cardiopulmonary distress with high mortality. Pulmonary involvement in European Puumala hantavirus (PUUV) infection has been reported, whereas knowledge of potential cardiac manifestations is limited. In Eurasia, hantavirus strains cause haemorrhagic fever with renal syndrome (HFRS), while hantaviruses in North and South America cause hantavirus pulmonary syndrome (HPS; denominated hantavirus cardiopulmonary syndrome), leading to severe and often fatal heart and lung failure [1,4,5,6]. Infection with the European Puumala hantavirus (PUUV) causes a mild HFRS, characterised by coagulopathy and acute renal failure [7]. Pulmonary involvement is very common in PUUV-infection, ranging from mild symptoms to severe lethal forms similar to HPS [8,9,10,11,12]. Echocardiographic data from PUUVinfected patients have mainly included information of morphological and visual descriptions of left ventricle function [9,19], with few details of right heart function that more likely would be influenced as a consequence of PUUV-related manifestations within the lungs

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