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A CHALLENGING CASE OF DILATED CARDIOMYOPATHY
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Abstract
A 49–years–old alcohol addicted man was admitted for worsening exertional dyspnoea. No cardiovascular risk factors were reported. On physical examination vesicular murmur was reduced on the right hemithorax. BP was 115/78 mmHg and oxygen saturation in room air was 91%, hence oxygen therapy was started. Blood exams showed elevation of the inflammatory markers. A CT scan showed a massive right pleural effusion. An EKG highlighted a normofrequent synus rhythm with a new left bundle branch block. A transthoracic echocardiography (ETT) revealed a dilated LV with severe systolic dysfunction (EF 15%) due to a diffuse hypokinesia, a large thrombus adherent to the middle segment of the antero–lateral wall (see attached images of apical three- and five-chamber, plus 3D reconstruction) and a severe RV dysfunction. In the Cardiac Intensive Care Unit he was started on an LMWH and diuretics. The day after, he developed a global aphasia and right hemiparesis: an ischemic stroke due to the occlusion of the right median cerebral artery was diagnosed through a CT angiography and an emergency mechanical thrombectomy was performed. After clinical stabilization, a coronary angiography showed no significant coronary artery stenosis and a cardiac magnetic resonance confirmed the diagnosis of dilated cardiomyopathy with severe impairment of the biventricular function, without evidence of late gadolinium enhancement (LGE). A right heart catheterization was consistent with a condition of post–capillary pulmonary hypertension with reduced cardiac index. During the hospitalization, the patient was kept on anticoagulant therapy, meanwhile switched to a VKA. Several echocardiographic controls documented the thrombus resolution, while the systolic function remained severely compromised. Genetic test for hereditary dilated cardiomyopathy turned out negative, therefore a diagnosis of alcoholic cardiomiopathy was made. The patient was discharged on dapaglifozin, as beta–blockers, ARBs and MRA were not tolerated due to hypotension. One month later the EF was 20%, hence the patient was scheduled for an ICD implantation. Alcoholic cardiomyopathy represents a common cause of dilated cardiomyopathy. Clinicians should be well aware of the possible life–threatening complications that can occur during the natural history of the disease, including acute heart failure, endoventricular thrombosis and embolization. Multimodality imaging is key for a correct diagnosis and a timely treatment.
Title: A CHALLENGING CASE OF DILATED CARDIOMYOPATHY
Description:
Abstract
A 49–years–old alcohol addicted man was admitted for worsening exertional dyspnoea.
No cardiovascular risk factors were reported.
On physical examination vesicular murmur was reduced on the right hemithorax.
BP was 115/78 mmHg and oxygen saturation in room air was 91%, hence oxygen therapy was started.
Blood exams showed elevation of the inflammatory markers.
A CT scan showed a massive right pleural effusion.
An EKG highlighted a normofrequent synus rhythm with a new left bundle branch block.
A transthoracic echocardiography (ETT) revealed a dilated LV with severe systolic dysfunction (EF 15%) due to a diffuse hypokinesia, a large thrombus adherent to the middle segment of the antero–lateral wall (see attached images of apical three- and five-chamber, plus 3D reconstruction) and a severe RV dysfunction.
In the Cardiac Intensive Care Unit he was started on an LMWH and diuretics.
The day after, he developed a global aphasia and right hemiparesis: an ischemic stroke due to the occlusion of the right median cerebral artery was diagnosed through a CT angiography and an emergency mechanical thrombectomy was performed.
After clinical stabilization, a coronary angiography showed no significant coronary artery stenosis and a cardiac magnetic resonance confirmed the diagnosis of dilated cardiomyopathy with severe impairment of the biventricular function, without evidence of late gadolinium enhancement (LGE).
A right heart catheterization was consistent with a condition of post–capillary pulmonary hypertension with reduced cardiac index.
During the hospitalization, the patient was kept on anticoagulant therapy, meanwhile switched to a VKA.
Several echocardiographic controls documented the thrombus resolution, while the systolic function remained severely compromised.
Genetic test for hereditary dilated cardiomyopathy turned out negative, therefore a diagnosis of alcoholic cardiomiopathy was made.
The patient was discharged on dapaglifozin, as beta–blockers, ARBs and MRA were not tolerated due to hypotension.
One month later the EF was 20%, hence the patient was scheduled for an ICD implantation.
Alcoholic cardiomyopathy represents a common cause of dilated cardiomyopathy.
Clinicians should be well aware of the possible life–threatening complications that can occur during the natural history of the disease, including acute heart failure, endoventricular thrombosis and embolization.
Multimodality imaging is key for a correct diagnosis and a timely treatment.
.
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