Winfried Krebs

Percutaneous transluminal coronary angioplasty immediately after intracoronary streptolysis of transmural myocardial infarction.

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 21 patients with acute myocardial infarction (AMI) treated by intracoronary infusion of streptokinase within 8 hours after the onset of symptoms. Streptolysis therapy began a mean of 3.6 1.2 hours (±± SD) after the onset of symptoms. The vessel was occluded in 14 patients and highly stenosed in seven. After the infusion of 67,300 ± 63,200 IU of streptokinase over 26.1 21.5 minutes, patency of the occluded vessels was reached. PTCA as performed 20-60 minutes after the end of streptokinase treatment in 19 patients and 24 and 31 hours after treatment in two patients. The dilation was successful in 17 patients (81%). The degree of vessel obstruction was reduced from 90.2 ± 7.3% to 58.6 19.5% (area method) and from 71.4 ± 12.4% to 39.2± 19.7% (diameter method). The improvement was 31.5 18.4% and 32.2 ± 19.3%, respectively. No reocclusion was induced by PTCA. Twenty patients were discharged. One died during hospitalization; at autopsy, the treated vessel was still patent. During the follow-up period, two reinfarctions and one asymptomatic reocclusion occurred. The clinical findings during the hospital course and the follow-up period were compared with those of a control group of 18 patients with AMI and comparable coronary stenoses who were treated only with streptokinase infusion. Four of these patients had a reinfarction during the hospital course, and three died during the follow-up period. PTCA can be performed safely and successfully immediately after intracoronary infusion of streptokinase in patients with AMI. By reducing the subtotal stenosis, this treatment contributes to the reperfusion of the ischemic myocardium, diminishes the risk of a reocclusion and seems to improve the prognosis.

Functional, angiographic and intracoronary doppler flow characteristics in symptomatic patients with myocardial bridging: Effect of short-term intravenous beta-blocker medication

OBJECTIVES We sought to define the effects of short-term beta-adrenergic blocking medication on intracoronary flow characteristics, clinical symptoms and angiographic diameter changes in patients with severe myocardial bridging of the left anterior descending coronary artery. BACKGROUND Controversy exists regarding the pathophysiology, clinical relevance and optimal therapy in symptomatic patients with myocardial bridges because antianginal drugs have not been systematically tested. METHODS In 15 symptomatic patients with myocardial bridging of the left anterior descending coronary artery, maximal lumen diameter reductions were evaluated by quantitative coronary angiography. There were no angiographic signs of coronary artery disease. Coronary blood flow velocities (using a 0.014-in. [0.035 cm] Doppler guide wire) were measured at rest, during atrial pacing and during intravenous administration of a short-acting beta-blocker (esmolol, 50 to 500 micrograms/kg body weight per min) with continuous atrial pacing. RESULTS The maximal angiographic systolic lumen diameter reduction within the myocardial bridges was 83 +/- 9% at rest, with a persistent diastolic diameter reduction of 41 +/- 11% (mean +/- SD). Short-term intravenous beta-blocker therapy decreased the diameter reduction during both systole (from 83 +/- 9% to 62 +/- 11%) and diastole (from 41 +/- 11% to 30 +/- 9%, both p < 0.001). The average diastolic peak flow velocity was higher within the myocardial bridges (33 +/- 13 cm/s) than the proximal (26 +/- 13 cm/s) and distal bridges (17 +/- 4 cm/s, both p < 0.001). During tachypacing, average diastolic peak flow velocity increased within the bridged segments to 63 +/- 21 cm/s versus 29 +/- 12 cm/s in the proximal and 20 +/- 4 cm/s in the distal bridges (both p < 0.001). Beta-receptor blockade produced a return to baseline values (average diastolic peak flow velocity within bridge 35 +/- 16 cm/s, p < 0.001). ST segment changes and symptoms were abolished with beta-blocker administration. CONCLUSIONS In patients with myocardial bridges, administration of short-acting beta-blockers during atrial pacing alleviates anginal symptoms and signs of ischemia. This effect was mediated by a reduction of vascular compression and maximal flow velocities within the bridged coronary artery segment.

Disturbed Intracoronary Hemodynamics in Myocardial Bridging Early Normalization by Intracoronary Stent Placement

BACKGROUND The purpose of this study was to evaluate the hemodynamic mechanisms leading to myocardial ischemia in patients with myocardial bridging. Myocardial bridging is known to induce angina and even severe myocardial ischemia. METHODS AND RESULTS In 12 symptomatic patients with myocardial bridges, quantitative coronary angiography was performed to obtain systolic/diastolic vessel diameters within the bridged segments. Coronary flow velocities, flow reserve, and pressures were determined with a 0.014-in Doppler and a 0.014-in pressure microtransducer. In 3 symptomatic patients, coronary stents were implanted and hemodynamic measurements were repeated immediately and after 7 weeks. An in vitro validation of the pressure measurements was performed. Angiography revealed a systolic diameter reduction of 80.6+/-9.2% and a persistent diastolic reduction of 35.3+/-11% within the bridged segment. Diastolic flow velocities (cm/s) were increased (31.5+/-14.3 within versus 17.3+/-5.7 proximal and 15.2+/-6.3 distal, P<.001). Coronary flow reserve distal to the bridge was 2.5+/-0.5. There was an increased peak systolic pressure within the bridged segment (171+/-48 versus 113+/-10 mm Hg proximal, P<.001). Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, the intracoronary peak systolic pressure, and clinical symptoms. Coronary flow reserve improved to 3.8+/-0.3. CONCLUSIONS Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.

Percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris: Analysis of early and late results

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 50 patients with stable and in 50 patients with unstable angina pectoris, each patient showing an isolated stenosis of more than 80% of the cross-sectional area of a single coronary artery. The technical success rate was 66% in the stable groups (26 of 37 patients [70%] with left anterior descending artery [LAD], 7 of 12 patients [58%] with right coronary artery [RCA]) and 74% in the unstable group (27 of 34 patients [79%] with LAD, 10 of 15 patients [67%] with (RCA). The increase in stenotic area in the unstable group exceeding that in the stable group for LAD stenoses (41.5 +/- 15.1% vs 32.3 +/- 14.5%, p less than 0.03), while in RCA stenoses the results in the stable group were better (45.1 +/- 17.6% vs 32.7 +/- 12.3%, n.s.). One acute vessel occlusion necessitating an emergency bypass operation occurred in each group (2%). The patient in the stable group died (total mortality rate 1%). Sixty-three of the successfully treated patients were routinely restudied 6 months later. According to clinical symptoms, 23% of the stable and 36% of the unstable group were in functional classes III and IV. From the anatomical viewpoint, a restenosis (greater than 85%) was found in 17% of the stable and in 24% of the unstable group. A further spontaneous decrease (greater than 10%) of the vessel obstruction was found in 47% of the stable group and in 12% of the unstable group.(ABSTRACT TRUNCATED AT 250 WORDS)

Three-dimensional echocardiographic determination of left ventricular volumes and function by multiplane transesophageal transducer: dynamic in vitro validation and in vivo comparison with angiography and thermodilution

The goal of this study was to validate 3-dimensional echocardiography by multiplane transesophageal transducer for the determination of left ventricular volumes and ejection fraction in an in vitro experiment and to compare the method in vivo with biplane angiography and the continuous thermodilution method. In the dynamic in vitro experiment, we scanned rubber balloons in a water tank by using a pulsatile flow model. Twenty-nine measurements of volumes and ejection fractions were performed at increasing heart rates. Three-dimensional echocardiography showed a very high accuracy for volume measurements and ejection fraction calculation (correlation coefficient, standard error of estimate, and mean difference for end-diastolic volume 0.998, 2.3 mL, and 0.1 mL; for end-systolic volume 0.996, 2.7 mL, and 0.5 mL; and for ejection fraction 0.995, 1.0%, and -0.4%, respectively). However, with increasing heart rate there was progressive underestimation of ejection fraction calculation (percent error for heart rate below and above 100 bpm 0.59% and -8.6%, P < .001). In the in vivo study, left ventricular volumes and ejection fraction of 24 patients with symmetric and distorted left ventricular shape were compared with angiography results. There was good agreement for the subgroup of patients with normal left ventricular shape (mean difference +/-95% confidence interval for end-diastolic volume 5.2+/-6.7 mL, P < .05; for end-systolic volume -0.5+/-8.4 mL, P = not significant; for ejection fraction 2.4%+/-7.2%, P = not significant) and significantly more variability in the patients with left ventricular aneurysms (end-diastolic volume 23.1+/-56.4 mL, P < .01; end-systolic volume 5.6+/-41.0 mL, P = not significant; ejection fraction 4.9%+/-16.0%, P < .05). Additionally, in 20 critically ill, ventilated patients, stroke volume and cardiac output measurements were compared with measurement from continuous thermodilution. Stroke volume as well as cardiac output correlated well to thermodilution (r = 0.89 and 0.84, respectively, P < .001), although both parameters were significantly underestimated by 3-dimensional echocardiography (mean difference +/-95% confidence interval = -6.4+/-16.0 mL and -0.6+/-1.6 L/min, respectively, P < .005).

Determination of left ventricular mass and circumferential wall thickness by three-dimensional reconstruction: In vitro validation of a new method that uses a multiplane transesophageal transducer☆☆☆★

Elevated left ventricular mass and increased wall thickness have important prognostic implications in clinical medicine. However, these parameters have been incompletely characterized by one- and two-dimensional echocardiography. Therefore this study was performed to validate in vitro measurement of left ventricular mass and circumferential wall thickness with a multiplane transesophageal transducer and three-dimensional reconstruction. Results for mass measurements were also compared with a standard method for the determination of left ventricular mass, the Penn convention. Fourteen necropsied left ventricles were scanned in a water bath by a volume-rendering, three-dimensional reconstruction system. There was an excellent correlation and high agreement for determination of three-dimensional left ventricular mass (r = 0.98; standard error of the estimate [SEE] = 9.6 gm; y = 1.02x + 0.46) and wall thickness (r = 0.93; SEE = 1.4 mm; y = 0.95x + 1.64) compared with anatomic measurements. Left ventricular mass by a simulated Penn convention revealed a lower correlation and larger error compared with three-dimensional measurements (r = 0.72; SEE = 42.8 gm; y = 1.01x + 9.61). Therefore determination of left ventricular mass by three-dimensional reconstruction was validated in vitro and was superior to one-dimensional echocardiographic methods.

EVALUATION OF REGIONAL SYSTOLIC FUNCTION IN HYPERTROPHIC CARDIOMYOPATHY AND HYPERTENSIVE HEART DISEASE : A THREE-DIMENSIONAL ECHOCARDIOGRAPHIC STUDY

Assessment of regional left ventricular (LV) function in patients with asymmetric LV hypertrophy is difficult with two-dimensional echocardiography mainly because of factors such as LV geometry, structure, regional wall stress, and ischemia. Multiplane transesophageal echocardiography with three-dimensional reconstruction of cross-sectional images was used for quantitative evaluation of regional wall thickness and fractional thickening. Fifteen patients (56 +/- 13 years old) with hypertrophic cardiomyopathy (LV ejection fraction 71% +/- 4%), 15 (62 +/- 13 years) with hypertensive heart disease (ejection fraction 66% +/- 8%) and 15 (53 +/- 11 years) healthy control subjects (ejection fraction 61% +/- 5%) were included in the analysis. Regional function was studied in four parallel equidistant short-axis cross sections from base to apex of the reconstructed left ventricle. In 15 degree intervals, 24 wall thickness measurements in each cross section were made at end-diastole and end-systole after endocardial and epicardial border tracing. A total of 192 measurements were obtained in each patient, and absolute wall thickening and fractional thickening were calculated. Absolute and fractional wall thickening showed a significant inverse relation to end-diastolic wall thickness in all heart conditions (r = 0.71, p < 0.0001). Regions of normal wall thickness in diseased patients were not hyperdynamic when compared with normal control subjects. Significant impairment in fractional thickening at identical end-diastolic thickness was observed in the septum compared with the lateral free wall in both hypertrophic cardiomyopathy and hypertensive heart disease. Thus regional systolic function is inversely related to end-diastolic wall thickness. The decrease in regional systolic function with increasing LV hypertrophy was similar in idiopathic and hypertensive cardiomyopathy. In both types of hypertrophy, significant differences in systolic function were observed in septal and lateral wall segments of similar wall thickness. This indicates that factors other than end-diastolic wall thickness influence myocardial thickening in patients with hypertrophy and preserved global function.

Hemodynamic effects of prenalterol in patients with ischemic heart disease and congestive cardiomyopathy.

SUMMARY The hemodynamic effects of a new,β agonist, prenalterol, were studied in 13 patients with severe left ventricular failure (New York Heart Association functional class III or IV). Seven patients had ischemic heart disease and six congestive cardiomyopathy. Left ventricular function was studied by catheter‐ tip manometer measurements of left ventricular pressure and simultaneous pressure‐volume analysis. To minimize rate‐related changes in left ventricular function, studies were performed during constant atrial pacing at 100 beats/min unless the intrinsic heart rate was higher. A 12‐mg i.v. dose of prenalterol was infused. The maximum rate of pressure development (peak positive dP/dt) increased from 1084 + 95 mm Hg/sec (mean + SEM) to 1493 ± 176 mm Hg/sec (p < 0.005). Stroke volume and ejection fraction also increased. Left ventricular relaxation, measured as the maximum rate of pressure fall (peak negative dP/dt) improved from −1011 ± 91 to −1202 ± 119 mm Hg/sec. Alteration in the time constant of pressure fall (T) also suggested improved relaxation, as it decreased from 71.8 ± 7.7 to 48.5 ± 6.3 msec. Prenalterol also decreased left ventricular stiffness, particularly in patients with very stiff ventricles. As a positive inotropic agent, prenalterol increased left ventricular mean power from 5.2 ± 0.4 to 6.8 ± 0.7 Wand left ventricular stroke work from 8.3 + 0.7 to 10.2 ± 1.0 W‐sec (p < 0.005). Left ventricular stress did not change significantly. The ratio of the diastolic pressure‐time index to the systolic pressure‐time index increased significantly (0.53 ± 0.04 and 0.63 ± 0.04, respectively, p < 0.005). Despite different absolute values, the percent changes of left ventricular function were similar in both groups. We conclude that even in patients with severe left ventricular failure, ventricular systolic and diastolic function can be improved by prenalterol. As a result of improved contractility, relaxation and stiffness, left ventricular filling pressure decreased. The data indicate a favorable effect on the balance between myocardial oxygen supply and demand. Intravenous prenalterol is a promising new drug for patients with severe heart failure.

Cardiovascular imaging by ultrasound

Part 1 Doppler assessment of valve and LV function 1. Part 2 Doppler assessment of valve and LV function 11. Part 3 New clinical frontiers of echocardiography 1. Part 4 New clinical frontiers of echocardiography 11. Part 5 Current application of TEE. Part 6 Future application of TEE. Part 7 Intravascular and intracardiac ultrasound imaging. Part 8 New technologies in ultrasound.

New echocardiographic and angiographic methods for right atrial volume determination: in vitro validation and in vivo results

Until now, right atrial (RA) volume calculation by means of two-dimensional echocardiography (2-DE) has only been attempted in a single plane: the apical four-chamber view. Our study reports a new method for RA volume calculation using two intersecting 2-DE views. For this purpose, silicone rubber casts of 19 human necropsy hearts were obtained and thin-walled natural rubber moulds of the RA casts were prepared. Totally filled with and immersed in water, the moulds could be visualized in the apical four-chamber view and an additional 2-DE plane, the latter corresponding to the subcostal view in vivo. In this view the vertical extension of RA could be estimated. Areas and lengths of RA were determined in the respective planes, and RA volume was calculated by applying the formula, area x length, to two intersecting planes. Finally, volume of the silicone casts was determined angiocardiographically (Angio) using a biplane method (30° RAO, 40° LAO-40° hepatoclavicular). The true RA volume was 106±23 ml (mean±1SD) as determined by water displacement. Using Angio an excellent correlation was found: the calculated volume amounted to 106±23ml; the difference was 5.5±4.8ml (n.s.); Angio vol=0.93 true vol+ 7.77; r=0.95; SEE= 7,4 ml. Volume determination from the apical four-chamber view of 2-DE using a monoplane disk method resulted in a mean volume of 62±17 ml. The mean difference to the true RA volume was 44±16 ml (p < 0.001). When volume calculations were made using the biplane method, a value of 105±22 ml resulted. The mean difference to true volumes was 7.4±4.8 ml: y=0.84x + 15.88; r=0.91; SEE=9.4 ml.In an in vivo study endsystolic RA volumes were calculated in a normal adult population (n=40) from the same intersecting planes as in vitro. A normal value of 38±6 ml/m2 was found. In vivo validation using Angio showed a slightly higher normal value of 43=7 ml/m2. Thus, 2-DE is highly accurate in determinating RA volume. In the in vitro as well as in the in vivo study the results of monoplane calculations are clearly inferior to a method which also takes account of the vertical extension of RA.