Christoph Spielberg

Effect on global and regional left ventricular functions by percutaneous transluminal coronary angioplasty in the chronic stage after myocardial infarction

Data are reported on 145 consecutive patients with prior myocardial infarction who had successful percutaneous transluminal coronary angioplasty (PTCA) of the infarct-related artery (5 +/- 6 months after infarction), and left ventricular (LV) angiograms before PTCA and during follow-up (7 +/- 4 months). There was a significant long-term improvement in LV function, ejection fraction increased from 60 +/- 13% to 64 +/- 13% (p less than 0.001), and regional wall motion abnormalities decreased by 40%. Multivariate discriminant analysis identified reduced LV function and a high degree of stenosis before PTCA as predictors for improvement in LV function (ejection fraction less than 60%: ejection fraction from 48 +/- 9% to 57 +/- 14%, p less than 0.001; and stenosis greater than or equal to 90%: ejection fraction from 59 +/- 15% to 66 +/- 14%, p = 0.003). Restenosis greater than or equal to 90% in patients with initial stenosis less than 90% decreased ejection fraction from 59 +/- 16% to 51 +/- 14% (p less than 0.05). Other factors tested (treatment of infarction by thrombolysis, time between infarction and PTCA, and severity of angina pectoris) had no effect on long-term changes in LV function. It is concluded that successful elective PTCA of a high-grade stenosis in an infarct-related artery may improve LV ejection fraction and regional wall motion abnormalities, especially in patients with impaired LV function.

Hemodynamic Response to Exercise-induced Myocardial Ischemia Detected by Transmitral Filling Patterns Derived from Doppler Echocardiography

There is still controversy as to the manner in which Doppler-derived transmitral filling patterns change because of myocardial ischemia. To evaluate the effects of exercise-induced ischemia on Doppler-derived filling patterns, 28 patients were examined at rest and during three stages of supine bicycle exercise (0.5, 1.0, and 1.5 W/kg). The peak early (E) and integrated early (Ei) and peak late (A) and integrated late (Ai) diastolic flow velocities, as well as their ratios (E/A, Ei/Ai), were compared between patients with exercise-induced ischemia but no wall-motion abnormalities at rest (ischemia group, n = 13) and those with akinetic scars from previous infarction but no exercise ischemia (scar group, n = 15). Normal subjects with no evidence of heart disease served as a control group (n = 11). At maximal workload the ischemia group showed a significantly lower peak flow velocity at atrial contraction than the control and scar group (0.74 +/- 0.18 vs 1.08 +/- 0.25 and 0.89 +/- 0.19 m/sec, respectively; p < 0.05) and also a significantly lower flow velocity integral at atrial contraction (8.24 +/- 2.2 vs 12.81 +/- 4.8 and 11.32 +/- 3.6 cm, respectively; p < 0.05). Therefore, the atrial contribution to filling was diminished during ischemia (36.2% +/- 9.2% vs 47.3% +/- 6.4% and 48.4% +/- 13.8%, respectively; p < 0.05). By maintaining the early filling rate during ischemia, the reduced atrial contribution resulted in a significantly higher E/A ratio (1.48 +/- 0.31 vs 1.05 +/- 0.15 and 1.16 +/- 0.44, respectively) and Ei/Ai ratio (2.0 +/- 1.06 vs 1.09 +/- 0.26 and 1.24 +/- 0.79, respectively). The assessment of Doppler-derived transmitral filling during exercise-induced ischemia shows mainly early diastolic filling, which is in contrast to the profile of impaired relaxation usually associated with ischemia. Evidence of exercise-induced ischemia leading to greater increases in left atrial pressure suggests that transmitral filling patterns are more closely related to hemodynamic status than to diastolic function.

Acute alterations of pre- and afterload: Are Doppler-derived diastolic filling patterns able to differentiate the loading condition?

The net effects of acute changes in pre- and afterload on left ventricular filling, were examined by altering loading conditions in normal subjects. The specific purpose of this study was to investigate whether Dopplerderived transmitral flow patterns are able to differentiate the type of loading conditions. In 24 normal subjects (13 females, 11 males, mean age 44.1±11.5 years), the following Doppler variables were determined at baseline, after rapid volume infusion (preload increase), after nitroglycerin administration (preload decrease), during isometric exercise (afterload increase), and after application of a converting enzyme inhibitor (afterload decrease): the peak and integrated early (E, Ei) and late (A, Ai) diastolic flow velocities, their ratios (E/A, Ei/Ai), the percentage of atrial contribution (ACON), and the acceleration and deceleration times (Ac, dc) of early filling. Reduced preload and increased afterload led to similar filling patterns characterized by a significant E and Ei decrease (p<0.05, compared to baseline) accompanied by an A and Ai increase with a resultant reduction of E/A and Ei/Ai. Both changes increased the atrial contribution to filling and reduced Ac and dc. Increased preload only significantly increased E and Ei, while reduced afterload did not induce any significant changes.Different loading conditions alter Doppler-derived diastolic filling patterns. However, the transmitral flow profile is not specific enough to distinguish the manner in which loading conditions have been altered.

Messung der Belastungshämodynamik im kleinen Kreislauf in der stationären Phase nach Myokardinfarkt: Eine zu Recht “vergessene” Untersuchung?

Bei 123 konsekutiven Patienten mit akutem Myokardinfarkt und systemischer Lyse wurde 7–10 Tage nach Infarkt in gleicher Sitzung wie der Linksherzkatheter auch ein Rechtsherzkatheter (RHK) mit ergometrischer Belastung durchgeführt. Nach 6 Monaten wurden beide Untersuchungen wiederholt. Es sollte untersucht werden, ob der RHK das Ergebnis der Koronarographie, d.h. das Vorliegen einer 1-, 2- oder 3-Gefäß-Erkrankung, das Ergebnis der Ventrikulographie, speziell die globale Ventrikelfunktion, und insbesondere den möglichen Profit von einer Intervention (PTCA/OP) beim Postinfarktpatienten voraussagen kann. Ergebnisse: 1. Ruhe- und Belastungshämodynamik korrelieren nicht zum Ausmaß der Koronarerkrankung. Es gibt jedoch eine Korrelation zwischen Belastbarkeit und Anzahl der stenosierten Koronarien. 2. Ruhe- und Belastungshämodynamik korrelieren nur schwach zur angiographischen Ventrikelfunktion. 3. Nur Patienten mit pathologischer Belastungshämodynamik profitieren von der Revaskularisation (definiert als Anstieg der Ejektionsfraktion > 5%). Dieser Profit ist allerdings eng zum Ausmaß der postinfarziellen Ventrikelschädigung korreliert. Folgerungen: Die individuelle Belastbarkeit kann einfach durch die Ergometrie erfaßt werden, die Ventrikelfunktion und damit das Ausmaß der postinfarziellen Ventrikelschädigung werden zuverlässig nichtinvasiv durch die Echokardiographie dargestellt. Die Belastungsuntersuchung mit RHK führt in der Planung der weiteren Strategie für den Postinfarktpatienten (insbesondere in der Frage nach der Notwendigkeit einer Koronarographie und evtl. Revaskularisation) nicht entscheidend weiter und ist u.E. deshalb verzichtbar. In 123 consecutive patients pulmonary hemodynamics at rest and during exercise were measured 7–10 days after acute myocardial infarction and systemic thrombolysis. Right- and left-heart catheterizations were performed at the same session and repeated after 6 months. We investigated if right-heart catheterization could predict the number of stenotic or occluded coronaries, the angiographic ventricular function and/or, most important, if the patient would profit from revascularization by PTCA or coronary surgery. Results: 1) Pulmonary hemodynamics at rest and during exercise did not correlate to the number of stenotic or occluded coronaries, but exercise tolerance did. 2) Correlation between ventricular function and pulmonary hemodynamics was weak. 3) Only patients with pathologically elevated pulmonary pressures at exercise showed profit from revascularization (increase of ejection fraction > 5% at control). This profit was closely correlated to the angiographic extent of ventricular damage. Consequences from our results: Individual exercise tolerance can easily be measured non-invasively. Ventricular function can be measured non-invasively as well as by echocardiography. Measurement of pulmonary hemodynamics at rest and during exercise does not contribute to planning the future management of the postinfarction patient and does not replace coronarography when indicated by clinical or non-invasive parameters.