Drug Therapy
Neurohumoral Therapy The term neurohumeral therapy refers to pharmacological modulation of pre- and afterload. One goal is to optimize pre- and afterload for both ventricles, aiming for the largest and most effective stroke volume. Another goal is minimization of pulmonary and peripheral congestion. For these purposes, ACE inhibitors, AT blockers, diuretics, and calcium antagonists are used. Especially in concurrent tachycardia, arterial hypertension, or severe heart failure, β-blockers are also prescribed in order to economize the cardiac workload. This management is very effective in mitral and aortic valve regurgitation and in intracardiac shunts due to atrial and ventricular septal defects. Such treatment is not particularly helpful in mitral stenosis and even less in aortic stenosis. Generally, neurohumoral therapy helps to bridge the time to surgical therapy, allowing to schedule surgery on a long-term basis.
Heart Rate and Blood Pressure Control Heart rate control is indicated in patients with tachycardiac atrial fibrillation, which is frequently observed in mitral valve disease and quite common in hypertrophic-obstructive cardiomyopathy. For optimal recompensation, hypotensive therapy should be particularly considered for patients with aortic regurgitation, but also in other valve disorders and intracardiac shunts. This type of pharmacological therapy is capable of avoiding or delaying cardiac overload and cardiac chamber dilatation.
Interventional Therapy Percutaneous Atrial Septal Device Closure Device closure of atrial septal defects includes closure of patent foramen ovale (PFO) and of secundum-type atrial septal defects (ASD II). All other types of ASDs remain the domain of surgery (see also
robotic surgery). Both types of intracardiac communication are transvenously closed through the right femoral vessels. In PFO closure, the interatrial communication is probed and a long guidewire introduced into the left superior pulmonary vein. Next, a long access sheath is inserted into the left atrium followed by implantation of the occluder device, which is released from the access sheath. The left-sided countercluder is opened first. After withdrawal of the whole system, the right-sided countercluder is opened in the right atrium. Before releasing the occluder from the delivery cable, transesophageal echocardiography (TEE) is employed to confirm proper placement of the device. This required only short-term sedation. Thereafter, the delivery cable is removed and the procedure finished.
In ASD device closure, some additional steps are required. Since defect size varies widely, ASD size must be determined with a sizing balloon, which is filled and withdrawn through the communication. During withdrawal, the balloon shows a waist, which is caused by the communication. Dimensions of this waist are measured by quantitative cineangiography and echocardiography. On the basis of balloon sizing, an adequate occluder size is selected. This maneuver as well as subsequent device implantation require echocardiographic guidance. In contrast to other centers, we use intracardiac echocardiography for this purpose.
