Philipp Kaufmann

Differentielle Bildgebung bei der Beurteilung der Mitralinsuffizienz

Differential imaging in the evaluation of mitral valve insufficiency In current clinical practice, choosing the optimal imaging technique for the quantification and differential diagnosis of mitral valve insufficiency constitutes a challenge, even for well-experienced cardiologists. This review article sought to identify the best possible method, or at least outline the most appropriate alternatives, depending on the context under discussion. Echocardiography, and particularly color Doppler imaging, still constitutes the method of choice for quantifying mitral valve insufficiency. While the major advantage of 3–dimensional (3D) echocardiography consists in its ability to accurately capture the often complex geometrical relationships involved, 2-dimensional (2D) echocardiography achieves higher temporal and spatial resolution. 2D echocardiography is the basic technique to evaluate cases of organic or functional mitral valve insufficiency. 3D transesophageal echocardiography (TEE) plays a significant role specifically in the peri-interventional or peri-operative setting. Cardiac magnetic resonance imaging (MRI) is an excellent technique for characterizing anatomical relationships, and represents the gold standard for assessing ventricular and atrial volumes. In addition, as it allows for blood flow to be directly quantified, cardiac MRI is considered the preferred alternative to echocardiography for the evaluation of mitral valve insufficiency. MRI is still, however, used to a limited extent in current clinical practice, owing to its relatively high cost and restricted availability. Computed tomography (CT) enables us to quantify both valvular regurgitation area and regurgitant volume. Due to the exposure to ionizing radiation and lack of blood flow quantification associated with this technique, its use in clinical practice is recommended only in exceptional cases, particularly for the combined assessment of coronary stenoses and mitral insufficiency. In the event of severe annular calcifications, CT can be used to both quantify the extent of valve calcification and identify the underlying pathology.

Erratum: Tetrahydrobiopterin restores impaired coronary microvascular dysfunction in hypercholesterolaemia (European Journal of Nuclear Medicine and Molecular Imaging (2005) 32 (84-91) DOI: 10.1007/s00259-004-1621-y)

PURPOSEnTetrahydrobiopterin (BH4) is an essential co-factor for the synthesis of nitric oxide (NO), and BH4 deficiency may cause impaired NO synthase (NOS) activity. We studied whether BH4 deficiency contributes to the coronary microcirculatory dysfunction observed in patients with hypercholesterolaemia.nnnMETHODSnMyocardial blood flow (MBF; ml min(-1) g(-1)) was measured at rest, during adenosine-induced (140 microg kg(-1) min(-1) over 7 min) hyperaemia (mainly non-endothelium dependent) and immediately after supine bicycle exercise (endothelium-dependent) stress in ten healthy volunteers and in nine hypercholesterolaemic subjects using 15O-labelled water and positron emission tomography. Measurements were repeated 60 min later, after intravenous infusion of BH4 (10 mg kg(-1) body weight over 30 min). Adenosine-induced hyperaemic MBF is considered to represent (near) maximal flow. Flow reserve utilisation was calculated as the ratio of exercise-induced to adenosine-induced hyperaemic MBF and expressed as percent to indicate how much of the maximal (adenosine-induced) hyperaemia can be achieved by bicycle stress.nnnRESULTSnBH4 increased exercise-induced hyperaemia in controls (2.96+/-0.58 vs 3.41+/-0.73 ml min(-1) g(-1), p<0.05) and hypercholesterolaemic subjects (2.47+/-0.78 vs 2.70+/-0.72 ml min(-1) g(-1), p<0.01) but had no influence on MBF at rest or during adenosine-induced hyperaemia in controls (4.52+/-1.10 vs 4.85+/-0.45 ml min(-1) g(-1), p=NS) or hypercholesterolaemic subjects (4.86+/-1.18 vs 4.53+/-0.93 ml min(-1) g(-1), p=NS). Flow reserve utilisation remained unchanged in controls (70+/-17% vs 71+/-19%, p=NS) but increased significantly in hypercholesterolaemic subjects (53+/-15% vs 66+/-14%, p<0.05).nnnCONCLUSIONnBH4 restores flow reserve utilisation of the coronary microcirculation in hypercholesterolaemic subjects, suggesting that BH4 deficiency may contribute to coronary microcirculatory dysfunction in hypercholesterolaemia.