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Pulmonary Hypertension in Left Heart Disease

Pulmonary Hypertension


Several forces contribute to the pathogenesis of pulmonary hypertension in patients with left-sided heart disease, with increased hydrostatic pressure leading to endothelial dysfunction and structural abnormalities in the pulmonary microcirculation as major contributors. Key events are breakage of the endothelial and alveolar basement membrane, with subsequent leakage of surfactant components into the systemic circulation.

How the balance of forces that causes permanent pulmonary vascular dysfunction is modulated, resulting in permanent pulmonary vascular disease in some patients, remains to be elucidated.

The cascade of events in heart failure that leads to pulmonary vascular disease ultimately affects right ventricular load and function, and leads to right ventricular failure and death.

Both systolic heart failure, and diastolic heart failure with preserved ventricular function may result in a variable degree of pulmonary hypertension. In diastolic heart failure, several pathogenetic mechanisms may play a role in an increasingly comorbid and elderly patient population.

In the intensive care setting, pulmonary hypertension associated with heart failure is a main target for a combination regimen of inotropic drugs (e.g. dobutamine, levosimendan) and vasodilators (e.g. NO and levosimendan).

There exist few controlled trials on classic pulmonary vasodilator treatments in chronic heart failure.

Conclusion:

Current data suggest that pulmonary hypertension associated with chronic heart failure is a mechanical complication of disturbed left ventricular filling. Given the predominantly negative trial results regarding classic pulmonary vasodilator drugs in PH associated with heart failure, off-label use of these drugs for PH associated with left heart failure is currently not justified. 

References


890-891-892-893

SessionTitle:

Pulmonary Hypertension in Left Heart Disease

Notes to editor


This congress report accompanies a presentation given at the ESC Congress 2008. Written by the author himself/herself, this report does not necessarily reflect the opinion of the European Society of Cardiology.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.