Valvular Heart Disease: Drug Therapy

Therapeutic target

Improvement in exercise capacity

Therapy recommendations

• Aortic stenosis (drug therapy is not possible).
• Aortic insufficiency:
  • ACE inhibitors, angiotension II receptor antagonists (to lower preload and afterload* ).
  • Cardiac glycosides (to increase contractility).
  • Diuretics
• Mitral stenosis:
  • Cardiac glycosides (for atrial fibrillation; to increase contractility/ability to contract).
  • Diuretics (diuretic medications).
• Mitral regurgitation:
  • Endocarditis prophylaxis (preventive medical measures designed to prevent infectious endocarditis).
  • Thrombosis prophylaxis in case of evidence of thrombi or thrombosis in the medical history.
  • In cardiac arrhythmias adequate therapy, if necessary ICD implantation (implantable cardioverter / defibrillator; pacemaker).
• Mitral prolapse:
  • Endocarditis prophylaxis
  • Thrombosis prophylaxis when there is evidence of thrombi (“blood clots”) or thrombosis (formation of a blood clot in a blood vessel) in the medical history (case history)
  • In cardiac arrhythmias adequate therapy, if necessary ICD implantation.
• See also under “Further therapy”.

* Preload (preload) – force that leads to the stretching of the fibers of the ventricles (heart chambers) at the end of diastole (relaxation and filling phase of the heart) Afterload (= afterload) – forces that counteract the contraction of the muscles of the heart chambers and thus limit the ejection of blood from the heart chambers into the vascular system.

Further notes

• Therapy of heart failure/heart failure (see below the topic of the same name).
• While NOAKs (non-vitamin K antagonist oral anticoagulants) can be used in all patients with valvular heart disease, patients with mechanical heart valves and those with rheumatic mitral valve stenosis should continue to receive VKAs (vitamin K antagonists).
• Congenital Heart Disease (synonym: congenital heart disease, AHF) and NOAKs: Adult patients with congenital heart disease on NOACs had higher rates of thromboembolism (3.8% versus 2.8%), MACE (7.8% versus 6.0%), bleeding (11.7% versus 9.0%), and all-cause mortality (4.0% versus 2.8%; all P <0.05) after 1 year of therapy compared with VKAs. CONCLUSION: VKAs should be considered more likely in patients with congenital heart defects.