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Updated: Jun 27, 2026

Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine
Published on: February 17, 2018
[64-year old patient with tachycardia and signs of heart failure]
M M Zaruba1, T Waggershauser, S Weckbach
1Medizinische Klinik I, Klinikum Grosshadern, Ludwig-Maximilians-Universität, Marchioninistrasse 15, Munich, Germany. Marc-Michael.Zaruba@med.uni-muenchen.de
Insights
Interventional occlusion of liver arterio-venous malformations successfully treated high cardiac output failure in a patient with Morbus Osler. This procedure reduced cardiac output by 25%, improving heart function and clinical stability.
Area of Science:
- Cardiology
- Interventional Radiology
- Hepatology
Background:
- High cardiac output failure can result from significant arterio-venous malformations (AVMs), posing a therapeutic challenge.
- Hereditary hemorrhagic telangiectasia (Morbus Osler) is associated with AVMs, including hepatic involvement.
Observation:
- A 64-year-old patient with Morbus Osler presented with severe right heart insufficiency due to hepatic AVMs.
- Medical therapy for high cardiac output failure was optimized but insufficient.
Findings:
- Interventional radiological occlusion of hepatic AVMs was performed in three sessions.
- The procedure resulted in a 25% reduction in cardiac output (from 20 L/min to 15 L/min).
- Transient elevation of transaminases was observed and proved reversible.
Implications:
- Interventional occlusion of hepatic AVMs is an effective treatment for high cardiac output failure in Morbus Osler patients.
- This approach can lead to reduced diuretic requirements and sustained clinical stabilization.
- Minimally invasive treatment of visceral AVMs can significantly improve cardiovascular outcomes.
Abstract:
We report on a 64-year old patient with known Morbus Osler and high cardiac output failure due to distinct arterio-venous malformations of the liver. Since the patient suffered from severe right heart insufficiency despite optimized medical therapy, we decided to conduct an interventional occlusion of the hepatic shunts in three single sessions. The transient elevation of transaminases was reversible. After interventional therapy cardiac output decreased from 20 l/min to 15 l/min (25%) leading to a reduction of diuretic dosage and a sustained stabilization of the clinical condition.
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