A 66 year-old man was admitted in emergency department of Tehran Heart Centre with recent exacerbation of progressive dyspnea aggravated as NYHA class II to III within a week earlier, malaise, dizziness, and perspiration. He was a known case of apical hypertrophic cardiomyopathy (HCM), persistent atrial fibrillation, and laryngeal squamous cell carcinoma diagnosed since 5 month earlier. He had received two courses of chemotherapy schedule followed by a regular period of local radiotherapy for 30 successive sessions. The patient had underwent coronary angiography, 8 months prior to admission which determined the presence of mild non-obstructive coronary artery disease. He had a history of heavy cigarette smoking as well as opium addiction. He also mentioned relatively regular use of Warfarin over 6 months prior to admission. Other medications prescribed earlier included furosemide 20 mg once a day, ASA 100 mg daily, and atorvastatin 20 mg once daily.
Initial vital signs revealed an irregularly irregular pulse (heart rate: 65 bpm), tachypnea (respiratory rate: 21/min), hypoxemia (pulse oxygen saturation: 88%), and low-grade fever recorded as 38.1 C0. Recorded blood pressure was 100/65 mmHg. The patient’s laboratory data on admission were as following:
WBC: 5000/mm3 (with 26.8% lymphocytes), haemoglobin: 13.1 gr/dl, platelet: 168,000/mm3, C-Reactive Protein (CRP):11.4 mg/L, INR: 2.43, creatinine: 1.3 mg/dl, magneseium: 1.5 meq/L, K: 4.2 meq/L.
A 12-lead electrocardiogram was obtained which showed the rhythm of atrial fibrillation accompanied with right bundle branch block, voltage criteria pertaining to left ventricular hypertrophy (LVH) denoting HCM, and non-specific ST depression with giant inverted T waves in precordial as well as in inferior leads (Fig. 1).
Transthoracic echocardiography demonstrated normal size and function of the left ventricle. Left ventricular ejection fraction (LVEF) was 60% with evident hypertrophy of all apical segments extending to mid part of the ventricle. Normal right ventricle (RV) size with moderate RV dysfunction were observed. Both atria were enlarged severely as measured by indexed volumes that were 65 ml/m2 and 57 ml/m2, respectively. There were also two large, fixed, wide based homogenous masses originating from left and right atria. Corresponding dimensions for the left atrial appendage mass and the other one attached to right atrial appendage were (50 × 24 mm) and (42 × 20 mm) respectively. Pulmonary artery pressure was found within normal range (PAP = 23 mmHg). Figure 2 illustrates the morphology and anatomic locations of the atrial masses.
A chest CT scan was performed which showed bilateral apical fibrosis in both lungs with peripheral patchy ill-defined ground glass densities in favour of COVID-19 pneumonia (Fig. 3).
The result of initial polymerase chain reaction (PCR) test for COVID-19 was positive. Thus, the patient received supportive medical care such as hydration with normal saline, non-invasive positive pressure ventilation (NIPPV), and hemodynamic monitoring. Intravenous unfractionated heparin was started immediately and he was treated with Hydroxychloroquine to reduce inflammation associated with COVID-19. Subsequent lab tests obtained during first week revealed elevated inflammatory markers. Increased levels of CRP, D-dimer and relative leukocytosis were detected. Values pertaining to CRP, D-dimer, and WBC were 14.6 mg/L, 2250 ng/ml, and 11,250, respectively.
Cardiac magnetic resonance imaging (CMR) revealed two large masses in left and right atrial appendages suggestive for thrombi (Fig. 4A).
A flare up episode of the disease occurred in the second week. However the inflammatory situation was managed conservatively without intubation. Then, symptoms, oxygen saturation and hemodynamic parameters improved gradually. Over the third week, a clinical steady state was achieved. After 14 days of treatment, COVID -19 PCR and chest CT scan were repeated. Although second PCR of the specimen via nasopharyngeal swab was negative but CT scan still showed residual parenchymal involvement of the lungs. Therefore, surgical operation was deferred about 35 days since initial visit. Since size of the clot did not change over a period of one month under stringent anticoagulation, and subsequent thromboembolism was likely, surgical removal was planned. Furthermore, watchful waiting in this situation is controversial and there is not enough high-quality evidence to support close observation or treatment of choice. Finally, the patient underwent open cardiac surgery, which resulted in excision of the two large atrial masses (Fig. 4B, C). Pathologic examination reported the presence of organized thrombus in combination with fibrosis, and interstitial tissue. The left atrial mass consisted of three pieces of grey-brownish elastic tissue totally measuring 60*50*20 mm, that were attached to each other. Further sectioning of both masses showed areas of yellowish discoloration and heterogeneous surfaces. The right sided mass appeared as a piece of cream-greyish elastic tissue with diameters of 50*25*20 mm. The patient had considerable recovery of signs, hemodynamic measures, while his symptoms improved significantly, until he was discharged 10 days after surgery. Total hospital stay was 45 days. In the first follow-up visit arranged 1 month after discharge, he seemed completely recovered. However, his functional capacity was still suboptimal and mild residual weakness was noticed. Second visit was set for 45 days later. All symptoms including scarce coughs finally disappeared.
