Matthias Vöhringer

Significance of Late Gadolinium Enhancement in Cardiovascular Magnetic Resonance Imaging (CMR)

Cardiovascular magnetic resonance imaging (CMR) permits optimal differentiation between normal and diseased myocardium with the use of gadoliniumbased contrast agents and special magnetic resonance pulse sequences. Imaging is performed 10–20 min after contrast agent application to produce so-called late gadolinium enhancement (LGE) images which depict diseased myocardium with excellent reproducibility. Areas showing LGE correspond to zones of myocyte necrosis or myocardial fibrosis as shown by comparison with histopathology. Typical patterns of hyperenhancement exist in ischemic heart disease but also in dilated cardiomyopathy, hypertrophic cardiomyopathy and other inflammatory or infiltrative myocardial disease and are described in this article. LGE-CMR is helpful to distinguish advanced ischemic heart disease from nonischemic dilated cardiomyopathy. In ischemic heart disease LGE can also predict the functional recovery after revascularization procedures by directly showing the remaining viable myocardium. LGE may also become useful to predict malignant arrhythmias in patients with ischemic heart disease or nonischemic cardiomyopathy. This may lead in future to an increased role of LGE-CMR as a prognostic tool.ZusammenfassungMit speziellen Magnetresonanzsequenzen (s. Abbildung 2) und Gadolinium-(Gd-)basierten Kontrastmitteln kann das sog. Late Gadolinium Enhancement (LGE) dargestellt werden (s. Abbildung 1). Eine relative Anreicherung von Gd und damit ein LGE entsteht, wenn im Rahmen einer akuten Nekrose myokardiale Zellmembranen rupturiert sind und damit das Verteilungsvolumen von Gd zunimmt. Zugrunde liegen kann aber auch bei chonischen Prozessen ein Rahmen des fibrotischen Umbaus vergrößerter extrazellulärer Raum im Myokard (s. Abbildung 3). Die verschiedenen myokardialen Erkrankungen führen zu unterschiedlicher, typischer Ausprägung von LGE (s. Abbildungen 5 bis 10). Aufgrund dieser krankheitstypischen Bilder kann LGE-CMR bei der Differentialdiagnose bei Patienten mit unklaren kardialen Krankheitsbildern, Herzinsuffizienz, Kardiomyopathien, Speichererkrankungen oder Myokarditis sehr nützlich sein. Zuverlässig kann z. B. eine fortgeschrittene ischämische Herzerkrankung von dilatativen Kardiomyopathien nichtischämischer Genese unterschieden werden. Die LGE-CMR bietet auch zunehmend Möglichkeiten zur individuellen Prognoseabschätzung. Anhand des transmuralen Ausmaßes von Infarkten lässt sich der von einer revaskularisierenden Maßnahme zu erwartende Gewinn abschätzen. Zunehmendes Interesse gilt der weiteren Charakterisierung des mit Ausmaß, Verteilung und Homogenität von LGE-Arealen (und damit von myokardialen Narben) verknüpften Risikos für das Auftreten maligner Rhythmusstörungen. Entsprechende Studien gibt es sowohl für ischämische als auch für dilatative und hypertrophe Kardiomyopathien. Eingang in die gültigen Leitlinien für entsprechende therapeutische Maßnahmen wie Implantation automatischer Kardioverter-Defibrillatoren haben diese Daten bisher noch nicht gefunden.

Incidence and predictors of permanent pacemaker implantation following transcatheter aortic valve implantation: Analysis from the german transcatheter aortic valve interventions registry

To determine predictors of permanent pacemaker (PPM) implantation up to 30 days after transcatheter aortic valve implantation (TAVI) in a prospective multicenter registry.

Oxygenation-sensitive CMR for assessing vasodilator-induced changes of myocardial oxygenation.

BackgroundAs myocardial oxygenation may serve as a marker for ischemia and microvascular dysfunction, it could be clinically useful to have a non-invasive measure of changes in myocardial oxygenation. However, the impact of induced blood flow changes on oxygenation is not well understood. We used oxygenation-sensitive CMR to assess the relations between myocardial oxygenation and coronary sinus blood oxygen saturation (SvO2) and coronary blood flow in a dog model in which hyperemia was induced by intracoronary administration of vasodilators.ResultsDuring administration of acetylcholine and adenosine, CMR signal intensity correlated linearly with simultaneously measured SvO2 (r2 = 0.74, P < 0.001). Both SvO2 and CMR signal intensity were exponentially related to coronary blood flow, with SvO2 approaching 87%.ConclusionsMyocardial oxygenation as assessed with oxygenation-sensitive CMR imaging is linearly related to SvO2 and is exponentially related to vasodilator-induced increases of blood flow. Oxygenation-sensitive CMR may be useful to assess ischemia and microvascular function in patients. Its clinical utility should be evaluated.

Cerebral and myocardial blood flow responses to hypercapnia and hypoxia in humans

In humans, cerebrovascular responses to alterations in arterial Pco(2) and Po(2) are well documented. However, few studies have investigated human coronary vascular responses to alterations in blood gases. This study investigated the extent to which the cerebral and coronary vasculatures differ in their responses to euoxic hypercapnia and isocapnic hypoxia in healthy volunteers. Participants (n = 15) were tested at rest on two occasions. On the first visit, middle cerebral artery blood velocity (V(P)) was assessed using transcranial Doppler ultrasound. On the second visit, coronary sinus blood flow (CSBF) was measured using cardiac MRI. For comparison with V(P), CSBF was normalized to the rate pressure product [an index of myocardial oxygen consumption; normalized (n)CSBF]. Both testing sessions began with 5 min of euoxic [end-tidal Po(2) (Pet(O(2))) = 88 Torr] isocapnia [end-tidal Pco(2) (Pet(CO(2))) = +1 Torr above resting values]. Pet(O(2)) was next held at 88 Torr, and Pet(CO(2)) was increased to 40 and 45 Torr in 5-min increments. Participants were then returned to euoxic isocapnia for 5 min, after which Pet(O(2)) was decreased from 88 to 60, 52 and 45 Torr in 5-min decrements. Changes in V(P) and nCSBF were normalized to isocapnic euoxic conditions and indexed against Pet(CO(2)) and arterial oxyhemoglobin saturation. The V(P) gain for euoxic hypercapnia (%/Torr) was significantly higher than nCSBF (P = 0.030). Conversely, the V(P) gain for isocapnic hypoxia (%/%desaturation) was not different from nCSBF (P = 0.518). These findings demonstrate, compared with coronary circulation, that the cerebral circulation is more sensitive to hypercapnia but similarly sensitive to hypoxia.

Exercise-Induced Spastic Coronary Artery Occlusion at the Site of a Moderate Stenosis Neither Prinzmetal's Angina nor Cardiac Syndrome X but “Prinzmetal X”

A 44-year-old man was referred to our hospital to undergo coronary angiography because of suspected coronary artery disease. For approximately 2 weeks, the patient had been experiencing typical symptoms of angina pectoris that occurred exclusively during physical exercise and predominantly in the morning hours when he bicycled to work. His general practitioner had performed a bicycle exercise test. In his written report, the practitioner noted that he suspected hemodynamically significant coronary artery disease because of reproduction of typical angina pectoris in addition to ischemic ECG changes. On admission, the patient was in good general condition with no symptoms at rest. Coronary angiography revealed an ≈80% stenosis in the small right coronary artery and an ≈50% stenosis in the proximal segment of the left anterior descending artery (LAD), although systolic left ventricular function was normal (Figure 1). Fractional flow measurements (fractional flow reserve) were performed in the right coronary artery and the LAD and revealed a significantly impaired fractional flow reserve only in the right coronary artery (fractional flow reserve 70%) and not in the LAD (fractional flow reserve 85%). Thus, the right coronary artery stenosis was treated with a drug-eluting stent (Figure 1), and the patient was discharged on medical therapy. Figure 1. Coronary angiograms of the left coronary artery (LCA) and right coronary artery (RCA) at first presentation. A stenosis of ≈50% was observed in the proximal segment of the LAD (left; black arrow), and an ≈80% stenosis was observed in the RCA (middle; black arrow). The stenosis of the RCA was stented successfully with a drug-eluting stent (right; black arrow). PCI indicates percutaneous coronary intervention. Six weeks later, the patient was referred again to our department because of unchanged symptoms of exercise-induced …

Contained aortic annulus rupture with persisting false aneurysm after transfemoral transcatheter aortic valve implantation

With older age and increasing comorbidities, conventional operative procedures for severe symptomatic aortic stenosis are associated with a high surgical risk. To date, transfemoral transcatheter aortic valve implantation (TF-TAVI) represents an accepted alternative method of intervention with a cardiovascular and all-cause mortality similar to operative replacement at early and long-term follow-up in this high risk population (Thomas et al., Circulation 124:425–433, 2011). Despite growing experience of the operators and improvement of the devices procedural and perioperative complications still occur (Panchal et al., Am J Cardiol, 2013). Aortic annulus rupture as well as the rupture of the membranous ventricular septum has been reported (Aminian et al., Catheter Cardiovasc Interv 81:E72–E75, 2013). We present the unusual case of an 80-year-old female who developed a false aneurysm following a contained aortic annulus rupture during a TF-TAVI procedure.

Primary cardiac lymphoma causing coronary vasospasm

A 63-year-old woman with no significant medical history or risk factors presented with an acute coronary syndrome. It was her first episode of angina pectoris (AP). ECG showed ST-segment elevations in II, III, and aVF, and cardiac biomarkers were negative. Coronary angiography revealed a severe stenosis in the right coronary artery (RCA) ( Panel A ), which disappeared after intracoronary nitroglycerin infusion. Subsequent coronary vasomotility testing with the intracoronary infusion of acetylcholine induced diffuse coronary vasospasm, reproducing …

Coronary Vasospasm: Is it a Myth?

This review addresses some myths about coronary vasospasm as the cause of angina pectoris. Coronary artery vasospasm is a common phenomenon, which is clinically encountered by busy cardiologists almost on a daily basis. It is the cause of resting angina in many patients without significant coronary artery disease, but also in patients with atherosclerotic coronary artery disease but no subtotal lesion. Although coronary artery vasospasm can be suspected clinically, proof cannot usually be obtained by non-invasive means but is easily available during cardiac catheterization. Patients with vasospastic angina are repeatedly exposed to this invasive procedure as most cardiologists suspect a coronary lesion requiring intervention as the cause of the patient’s resting angina. Adding an intracoronary acetylcholine test to the catheterization procedure may establish the correct diagnosis and enable treatment with calcium antagonists and nitrates. Epicardial vasospasm may be observed during the test in patients with and without angiographically visible lesions in the coronary arteries. Almost 50% of all pathological tests, however, do not show epicardial vasospasm but reproduction of symptoms and electrocardiogram signs of ischemia indicating spasm of the microvessels.

Assessment of coronary endothelial function using blood oxygenation level dependant cardiovascular magnetic resonance imaging (BOLD-CMR) in a canine model.

Background Endothelial function is important in the pathogenesis of atherosclerosis. Whereas endothelial function of peripheral circulation can be assessed non-invasively with Flow-Mediated Dilatation, no method exists for coronary circulation. BOLD-CMR utilizes inherent contrast, where the signal intensity (SI) is linearly correlated with the regional tissue level of deoxygenated hemoglobin. This technique may have potential to assess coronary endothelial function non-invasively.

Assessment of myocardial perfusion reserve with blood oxygen level-dependent cardiovascular magnetic resonance imaging

Background: New Blood Oxygen Level-Dependent Cardiovascular Magnetic Resonance Imaging (BOLD-CMR) sequences show a high sensitivity and consistent image quality that allows for assessing tissue oxygenation. We hypothesized that BOLD-CMR can quantitatively assess myocardial blood flow changes using myocardial oxygenation as a biomarker. Objective: To test whether a BOLD-CMR sequence accurately estimates myocardial perfusion changes. Methods: Six anesthetized mongrel dogs were instrumented with a coronary infusion catheter in the circumflex coronary artery (LCX), an MR-compatible epivascular flow probe around the LCX and a catheter in the coronary sinus. Using a clinical 1.5 T MRI system (MAGNETOM Avanto, Siemens Healthcare, Germany), SSFP BOLD-CMR was performed during graded intracoronary infusion of adenosine in the LCX. Typical scan parameters were: Field-of view (FOV) 190x280 mm; matrix size 106x192; slice thickness 10 mm; TR/TE 5.8/2.9 ms; flip angle 90o; typical breath-hold duration 14s. Images were analyzed using clinically validated software (cmr, Circle Cardiovascular Imaging Inc., Calgary, Canada) and the BOLD signal intensity (SI) for each was calculated. Correlations of coronary flow, oxygen saturation in the coronary sinus and myocardial BOLD-CMR signal intensity (BOLD-SI) changes were calculated by regression analysis. The same CMR imaging protocol was used in 11 healthy volunteers (6 male, 5 female) before, during and after intravenous adenosine infusion (140 ⎧g/kg). Myocardial perfusion reserve in the human volunteers was calculated from flow measurement in the coronary sinus using velocity-encoded CMR. Results: In dogs, adenosine-induced blood flow changes in the LCX agreed very well with changes in coronary venous saturation (logarithmic scale, r=0.94, p<0.001). Furthermore, coronary venous saturation showed a strong yet linear correlation with BOLD-SI changes (r=0.80, p<0.001). Consequently, as shown in Figure 1, blood flow changes correlated very well with the BOLD-SI (r=0.84, p<0.001). The exponential correlation is described by the equation (y) = 98.3+25.4*(1-e) (x=flow, y=BOLD-SI). In the volunteers, adenosine infusion resulted in a significant myocardial perfusion increase (416±69% of baseline, p<0.001). BOLD SI increased significantly by 20.1±9.5% (p<0.001 as compared to baseline). The reproducibility of the BOLD-SI in the two baseline measurements before and after adenosine infusion was excellent (mean difference 0.1±2.6%, p=0.97). Conclusion: State-of-the-art BOLD-sensitive MRI sequences detect changes of myocardial perfusion in an experimental animal model and in humans in vivo. This technique may allow for an accurate, non-invasive assessment of myocardial perfusion reserve in humans.