Research Information System
Uluslarası Akademik Geriatri Kongresi, Antalya, Turkey, 12 - 16 April 2017, pp.100-101
INFLUENZA A VIRUS INFECTION TRIGGERING
MYOCARDIAL INFARCTION AND ACUTE HEART
FAILURE
Utku Zor1, Hülya Kuşoğlu2
1
Acibadem Fulya Hospital,cardiology
2
Acibadem Univesity School of Medicine,ınfectious Diseases And Clinical Microbiology
Introduction: Influenza infection can lead to serious complications
in people having underlying medical disorders such as cardiovascular
diseases. It is known that Influenza viruses have direct effect on the
myocardium and can also lead to exacerbations of existing cardiovascular diseases. Geriatric patients are at high risk of morbidity and
mortality during an Influenza infection.
Case presentation: An 85-year-old woman was admitted to the
hospital with fever, chest pain and shortness of breath present for
2 days. Her past medical history included coronary artery disease,
aortic valve stenosis, hypertension, hyperlipidemia and hypothyroidism. She underwent a coronary artery by-pass and a bioprosthetic
valve replacement operation 4 years ago. Her physical examination
revealed tachypnea with breaths 34/minute. Respiratory sounds were
compatible with paninspiratory rales blaterally at lower and mid regions. At room air her O2 saturation rate was 85%. Cardiovascular
assessment showed jugular venous distention, a S4 gallop rhythm, an
apical 3/6 pansystolic murmur, an aortic 2/6 systolic ejection murmur.
Her blood pressure was to be 158/60 mmHg, heart rate was 112
beats/min. Pretibial edema was observed. Her chest X-ray showed bilateral pulmonary vascular cephalization, infiltrates suggesting alveolar edema. ECG revealed pathological Q-waves on the inferior
derivations, a 1-mm- ST depression on the precordial leads V4,V5
and V6. Echocardiography revealed a decrease in her left ventricular
ejection fraction rate of 40% (N: >55%) which was known to be
55-60% on her previous Echocardiography. Basal inferolateral wall
was akinetic as before but severe basal and mid anterolateral motion hypokinesia were new findings. The mitral valvular structure was
normal, but severe functional mitral regurgitation was seen. The bioprosthetic aortic valve was functioning normally. Her first laboratory
results showed a Troponin I as 3.066ng/mL (N:<0.04);NT Pro BNP
7340 pg/mL (N:<738). A rapid Influenza testing resulted positive for
Influenza A. With these findings the patient was admitted to the Intensive care unit with the diagoses of acute coronary syndrome and
acute heart failure, developed during an influenza infection. Mechanical ventilation was performed and she was given acetylsalycylic acid,
ticagralor, nitroglycerin and furosemide infusion. Enoxaparin was
started after her INR level dropped below 2.0. Influenza infection was
treated with oseltamivir for 5 days. Her previous angiography was
re-assessed;many lesions which were not amenable to revascularization and supplying the newly diagnosed hypokinetic regions were determined. A new angiography was not performed, with the decision
of continuing medical therapy.
Discussion: This case is a good example of increased risk for cardiovascular mortality and morbidity during influenza infections and
emphasizes the role of Influenza vaccination in vulnerable patients
such as those with coronary artery disease.
Keywords: Acute myocardial infarction, Acute heart failure, Influenza
infection