[t-PA in thrombolytic therapy of acute myocardial infarct]. / t-PA zur thrombolytischen Therapie des akuten Herzinfarkts.

In the past decade, thrombolytic therapy has become standard treatment of acute myocardial infarction. When the importance of thrombosis in the pathogenesis of acute infarction was fully recognised, several plasminogen activators were developed, streptokinase, urokinase, recombinant tissue-type plasminogen activator (t-PA, alteplase), anistreplase and saruplase (prourokinase). Thrombolytic agents are plasminogen activators which possess as a common characteristic the ability to activate plasminogen to plasmin, and result in fibrinolysis and varying degrees of depletion of circulating fibrinogen, factor V and factor VIII. A lot of animal experiments provided the basis for the rationale that recanalisation and reperfusion early in the course of myocardial infarction would limit myocardial necrosis, improve left ventricular function, and improve patient outcome. Native tissue plasminogen activator is normally secreted by vascular endothelium and the most important property of the drug is its relative fibrin specificity. Fibrin strikingly increases the rate of conversion of plasminogen to plasmin by t-PA. The isolation of the complementary DNA coding for t-PA, its insertion into the genome of Chinese hamster ovary cells, and its expression in suspension cultures of these cells have facilitated the large-scale production of t-PA, making it available as a drug for the treatment of acute myocardial infarction. A variety of dosage schemes have been used for alteplase, the standard schedule has been 100 mg given over 3 hours. Higher doses and faster administration (accelerated, front-loaded) are associated with higher patency rates. Alteplase has generally but not always been shown to have higher reocclusion rates than the non-fibrin-specific plasminogen activators. Reocclusion has been shown to be associated with adverse clinical outcome. Therefore, the rate of reocclusion is considered an important measure in evaluating thrombolytic regimens. The combination of alteplase with either urokinase or streptokinase has resulted in early patency rates comparable to alteplase alone, and low rates of reocclusion. Large, randomised clinical trials have demonstrated that thrombolytic therapy reduces mortality significantly in patients with ST elevation treated within the first 6 to 12 hours of acute myocardial infarction. As compared to an overall reduction of mortality with thrombolytic treatment, neither the GISSI-2/international trial nor the Third International Study of Infarct Survival (ISIS-3) trial of more than 60,000 patients found a difference in associated mortality between the use of streptokinase and the use of t-PA, or between the use of these agents and that of anistreplase. The addition of subcutaneous heparin to the regimens did not significantly reduce mortality as compared with no use of heparin.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibacterial efficacy of ciprofloxacin in a case of endocarditis due to Cardiobacterium hominis.

Endocarditis due to Cardiobacterium hominis is rare and may be treated with a variety of antibiotics. We isolated the bacteria from blood cultures of a patient with Cardiobacterium hominis endocarditis who could be successfully treated with ciprofloxacin. The bacterial features of Cardiobacterium hominis are presented, and susceptibility to ciprofloxacin is documented with bacterial killing curves employing peak and trough specimens of patient's serum.

Left ventricular hyperkinesis in acute myocardial infarction and at control angiography after 1 month.

One-hundred-and-fifty-four consecutive patients were treated with intravenous and intracoronary streptokinase within 3 h of the onset of acute myocardial infarction. Left ventricular function was determined from contrast ventriculograms obtained in the acute phase and at follow-up at 28 (15-37) days in 123 patients with matched ventriculograms. Regional wall motion analysis was performed with a radial axis system and asynergy determined by comparing percentage radial shortening with findings in ten normal controls. Reperfusion was achieved in 79% of patients. However, there was no significant difference in global ejection fraction between the acute phase (60.6%) and follow-up (60.4%) ventriculograms, although a significant reduction of hypokinetic areas was seen. An increase in regional ejection fraction in anterior (+10%) and inferior (+9%) hypokinesis was counterbalanced by a reduction of incidence (-11%) of hyperkinesis and regional ejection fraction (-10%) in the contralateral wall. In patients with a patent infarct-related vessel at follow-up, no difference in global or regional parameters was found in the acute phase, but at follow-up these patients showed improved regional wall motion with an increase in global ejection fraction (1.6%, n.s.). In patients with occluded vessels at follow-up global ejection fraction decreased (-5.4%, P less than 0.05). The decrease of frequency and extent of hyperkinesis in the clinical course of acute myocardial infarction tends to counterbalance recovery of wall motion in the infarcted region, resulting in little change in global ejection fraction.

[Scintigraphic quantification of pulmonary pressure increase in mitral valve stenoses based thallium uptake by the lung]. / Szintigraphische Quantifizierung der pulmonalen Druckerhöhung bei Mitralstenosen durch den Lungen-Thallium-Uptake.

30 patients (24 fm, 6 m) with angiographically proven mitral stenosis as well as 10 healthy controls were investigated by wedge catheterism and thallium-201-scintigraphy to calculate the heart-lung quotient of the isotope. All patients with mitral stenosis could be discriminated from controls by a pathological increase of isotope concentration in the lungs. 4 groups could be subdivided: the first consisted of 8 patients with normal pulmonary artery pressure of x = 13.06 mm Hg and a normal heart-lung quotient less than 1.1. The second group of 15 patients showed passive pulmonary hypertension with a PAm of x = 27.57 mm Hg and heart-lung quotients between 1.1 and 1.4. A third group of 9 patients showed PAm of 36.76 mm Hg with reactive hypertension and a HLQ between 1.4 and 1.6. The last group of patients showed pulmonary hypertension of x = 45 mmHgPAm and a heart-lung quotient of greater than 1.6. Scintigraphy alone allowed classification of the patients, so the value of this method is proven for pre- and postoperative strategy.

Imaging of acute myocardial infarction by magnetic resonance tomography (MRT) using the paramagnetic relaxation substance gadolinium-DTPA.

Twenty-six patients admitted to the Free University of Berlin University Hospital catheterization laboratory with acute myocardial infarction were studied. The diagnosis was confirmed by angiography, but acute revascularization was unsuccessful in every case. MR imaging was performed within 7 days of the acute event in 11 patients with uncomplicated clinical courses after acute infarction. Imaging was performed within 3 weeks in three additional cases, while the remaining 12 patients underwent studies more than 3 weeks after infarction. We determined signal intensity at three points within the area of infarction and at three other points in adjacent myocardial tissue. Decreased signal intensity within the area of infarction was found in native scans in 60% of all cases. Administration of gadolinium-DTPA 0.1 mmol/kg body weight was followed by a mean 70% increase in signal intensity within the zones of acute infarction, as compared to a 20% increase in surrounding myocardial tissue. In cases of subacute and chronic infarction, there was no significant signal enhancement after administration of gadolinium-DTPA. Uptake of the substance in the area of acute infarction may be a positive marker of acute myocardial necrosis and as such may prove useful in the clinical setting.

Regression of left ventricular hypertrophy under ramipril treatment investigated by nuclear magnetic resonance imaging.

Thirty-two hypertensive subjects with diastolic blood pressure greater than 95 mm Hg were treated with ramipril over a period of 3 months. To determine the effective decrease of blood pressure and for reliable and reproducible demonstration of regression of myocardial hypertrophy during ramipril treatment, we performed parallel measurements with magnetic resonance imaging (MRI) and echocardiography. Measurements were carried out before treatment, 4 h after the first dose, and after 14 days and 3 months of treatment. MRI slices showed a significant decrease of interventricular septal thickness from 19.57 to 15.20 mm, whereas echocardiography demonstrated an equivalent decrease from 18.78 to 14.57 mm. At each measuring point, quantification of wall thickness was performed three times and the means were calculated. The septum and the posterior wall of the left ventricle were also measured at three different points. The values were obtained with negligible scatter and the changes with ramipril treatment were highly significant (p less than 0.001). A concomitant decrease of blood pressure was also observed. The therapeutic aim to reduce diastolic blood pressures below 90 mm Hg was achieved in all patients. In addition to the significant reduction in blood pressure, the angiotensin converting enzyme (ACE) inhibitor ramipril caused a significant regression of pathologic left ventricular hypertrophy demonstrated by magnetic resonance imaging and echocardiography.

[Lung thallium uptake for non-invasive assessment of increased pulmonary pressure in mitral valve stenosis]. / Der Lungenthallium-Uptake zur nichtinvasiven Abschätzung der pulmonalen Druckerhöhung bei Mitralstenose.

30 patients (24 females, 5 males) with angiographically proven mitral stenosis as well as 10 healthy controls were investigated by wedge catheterism and thallium-201-scintigraphy to calculate the heart-lung quotient (HLQ) of the isotope. All patients with mitral stenosis could be discriminated from controls by a pathological increase of isotope concentration in the lungs. 4 groups could be subdivided: the 1st group consisted of 21% of the patients with normal pulmonary artery pressure of x = 13.06 mm Hg and a normal HLQ less than 1.1. The 2nd group of 39% of the patients showed passive pulmonary hypertension with a PAm of x = 27.57 mm Hg and HLQ between 1.1 and 1.4 A 3rd group showed PAm of 36.76 mm Hg with reactive pulmonary hypertension and a HLQ between 1.4 and 1.6. The last group showed pulmonary hypertension of x = 45 mm Hg PAm and a HLQ of greater than 1.6. Scintigraphy alone allowed classification of the patients, so the value of this method is proven for pre- and postoperative strategy.

[Comparative clinical studies of myocardial blood flow in coronary heart disease with two nifedipine preparations]. / Klinische Vergleichsuntersuchungen zur Myokarddurchblutung bei koronarer Herzerkrankung mit zwei unterschiedlichen Nifedipin-Zubereitungen.

Clinical, ergometric and scintigraphic examinations were performed before and after oral administration of a commercially available nifedipine preparation used as a standard (reference preparation; dosage: 3 x 10 mg/d) in 21 patients with angiographically verified coronary artery disease. In an open comparison study the same parameters were investigated after a 4 week course of a different nifedipine preparation as a test preparation (Corotrend; dosage: 3 x 10 mg/d). The study was performed in order to determine whether there were quantitative differences in myocardial microperfusion when different galenical preparations of nifedipine were used. There were no statistically significant differences between the two nifedipine preparations in the test parameters recorded. Both substances were associated with highly significant increases in microperfusion as compared to findings in the washout phase. Clinical effects on incidence of chest pain and on reductions in blood pressure were comparable. Patients demonstrated slightly better exercise tolerance with the reference agent, and computerised impulse-rate analysis of the tomoscintigrams demonstrated somewhat better microperfusion with this drug, though the differences between the two agents did not attain statistical significance. As the result of this analysis the two drugs would appear to be equivalent in clinical potency.

Microperfusion in coronary artery disease under treatment with the calcium antagonist gallopamil.

The calcium antagonistic principle, i.e. the inhibition of calcium influx into the heart muscle cell and smooth muscle cell, in this particular case gallopamil as an example of a drug with this principle of action, can certainly be regarded as one of the most important concepts in modern coronary therapy. On account of the increase of myocardial perfusion, which is ascribed to this calcium antagonist, gallopamil may be administered as an adjunct to postoperative therapy. It is even a drug alternative to bypass grafting. Previous investigations of the ST segment and subjective ischemic parameters have not always shown coherent findings. The purpose of this study was to objectify clinical improvement after therapy with gallopamil (Procorum) by means of reliable methods and reproducible measurements. Myocardial perfusion was analysed in 31 patients by longitudinal tomoscintigraphy before and after therapy with 2 x 2 mg gallopamil intravenously and 6 weeks at 3 x 50 mg/d orally followed by placebo control. The computerized circumferential mapping of impulse rates showed a significant increase of impulse density in ischemic segments after both intravenous and oral therapy with gallopamil.

[Results and limits of fibrin-unspecific thrombolysis in acute myocardial infarct]. / Ergebnisse und Grenzen einer nicht fibrinspezifischen Thrombolyse beim akuten Herzinfarkt.

Acute myocardial infarction is caused by thrombotic occlusion of a coronary vessel. Mortality and quality of life are both determined by the extent of infarction. It is possible to interrupt the development of necrosis by early fibrinolytic therapy. If reperfusion is initiated within three to six hours, a significant reduction in mortality is likely. Currently available fibrin-unspecific plasminogen activators such as streptokinase and urokinase are effective thrombolytic agents but do not fulfill all the criteria of an ideal plasminogen activator. Recanalisation rates are relatively low after intravenous administration, since the agents are not fibrin-specific and because the effect is delayed. Serious hemorrhagic complications may occur, since therapeutically effective dosage results in a hemostatic defect. The possible advantages of reduction in blood viscosity for collateral circulation in the ischemic region and a possible antithrombotic effect have not been defined. A complex strategy is necessary for optimal treatment of acute myocardial infarction. Early intervention is decisive in regard to recanalisation rate, infarct size, left ventricular function and mortality, while delayed interventions serve to maintain the advantages of early recanalisation by limiting angina pectoris and preventing reinfarction. Therefore, a combination of early intravenous administration of a fibrinolytic agent with subsequent invasive intervention appears reasonable and advantageous. Progress in the treatment of acute myocardial infarction will depend on development of effective plasminogen activators capable of achieving rapid and complete recanalisation without major side effects after intravenous administration.

[Effect of a secretolytic and a combination of pinene, limonene and cineole on mucociliary clearance in patients with chronic obstructive pulmonary disease]. / Einfluss eines Sekretolytikums und einer Kombination von Pinen, Limonen und Cineol auf die mukoziliare Clearance bei Patienten mit chronisch obstruktiver Atemwegserkrankung.

Effect of a Secretolytic and a Combination of Pinene, Limonene and Cineole on Mucociliary Clearance in Patients with Chronic Pulmonary Obstruction. Studies demonstrating the elimination of radioactive particles during a 7-day course of therapy with 3 x 30 mg ambroxol or 4 x 1 capsule. Gelomyrtol forte (1 capsule = 0.3 g Myrtol, standardised to at least 20 mg of alpha-pinene, 75 mg of limonene and 75 mg of cineole (eucalyptol) yield improved mucociliary clearance in both groups. No change of lung function was observed.

Residual coronary stenosis after thrombolysis with rt-PA or streptokinase: acute results and 3 weeks follow-up.

Ninety-one patients with acute myocardial infarction were assigned to intravenous treatment with streptokinase or rt-PA as part of the randomized trial carried out by the European Study Group for Recombinant Tissue-Type Plasminogen Activator (rt-PA). A patent coronary artery was found in 37 of 45 (82%) patients treated with rt-PA and in 27 of 46 (59%) patients treated with streptokinase 75-90 minutes after start of infusion. Patients were subsequently anticoagulated with heparin or dicoumarol up to a repeat angiography 3 weeks after the infarction. Of the 64 patients with successful reperfusion, 3 died and 3 suffered reocclusion of the vessel. Quantitative analysis of the coronary stenosis both immediately after thrombolysis and at 3 weeks follow-up was possible in 33 cases. Residual stenosis (percentage narrowing of diameter) decreased from 74 +/- 14% to 56 +/- 17% (P less than 0.05). No difference was observed between the groups of patients treated with streptokinase (74 +/- 9% to 57 +/- 12%, N = 17) and with rt-PA (74 +/- 17% to 56 +/- 21%, N = 16). Despite the significant regression, a coronary stenosis of more than 50% of the diameter persisted in 82% of the patients three weeks after the infarction.

Use of nuclear magnetic resonance imaging to show regression of hypertrophy with ramipril treatment.

Thirty-two patients with arterial hypertension (diastolic blood pressure greater than 95 mm Hg) were treated with ramipril for 3 months. The aim of the study was to achieve an effective decrease in blood pressure and demonstrate reliably and reproducibly that regression of left ventricular hypertrophy takes place with ramipril treatment. Nuclear magnetic resonance images and echocardiographic measurements of the left ventricle were therefore made before treatment started, 4 hours after the first dose, 14 days after the start of treatment and after 3 months of treatment. The thickness of the septum decreased from 19.57 to 15.20 mm on magnetic resonance scans and from 18.78 to 14.57 mm on echocardiograms. The values were reproduced 3 times at the same measuring point and means were calculated. The septum and posterior wall of the left ventricle were also measured at 3 different points. With negligible scatter, the values obtained were reproducible and the differences were highly significant (p = 0.001). A parallel decrease in blood pressure to levels 15% below baseline was also observed. The therapeutic aim of achieving diastolic blood pressure levels of less than or equal to 90 mm Hg was achieved in all patients. In addition to reducing the blood pressure significantly, the angiotensin converting enzyme inhibitor ramipril caused a significant regression of pathologic left ventricular hypertrophy, which was demonstrated clearly using magnetic resonance imaging and echocardiography.

Magnetic resonance imaging (MRI) in different stages of myocardial infarction using the contrast agent gadolinium-DTPA.

We investigated 26 patients admitted to our catheterization laboratory with a diagnosis of acute myocardial infarction. In each case acute revascularization was unsuccessful, but the diagnosis was confirmed by angiography. In 11 patients with an uncomplicated course of acute myocardial infarction magnetic resonance imaging was carried out within 7 days of the acute event. In three additional cases imaging was performed within 3 weeks, while a remaining 12 patients underwent studies more than 3 weeks after the onset of symptoms. We determined signal intensity at three points within the area of infarction and at three other points in adjacent myocardial tissue. Decreased signal intensity within the area of infarction was present in native scans in 60% of all cases. Application of 0.1 mmol/kg body weight gadolinium-DTPA was followed by an average 70% increase in signal intensity within zones of acute infarction, as compared to a 20% increase in surrounding myocardial tissue. In cases of subacute and chronic infarction there was no significant signal enhancement after administration of gadolinium-DTPA. Uptake of gadolinium-DTPA in the area of acute myocardial infarction may be a positive marker of acute myocardial necrosis, which may be of potential clinical benefit.

[Experimental studies of the evaluation of the size of infarct and perfusion defects using analysis of regional wall motion from 2-dimensional echocardiography]. / Experimentelle Untersuchungen zur Beurteilung der Infarkt- bzw. Perfusionsdefektgrösse mittels regionaler Wandbewegungsanalyse aus dem zweidimensionalen Echokardiogramm.

In an experimental study with laboratory animals we studied the relation between the extent of a disorder of regional wall motion as determined by echocardiography and size of a perfusion defect following occlusion of a coronary vessel for 5 hours. It was demonstrated that wall motion is not uniform in a normal left ventricle and that there is a wide range of variability in wall motion within a given myocardial segment. For this reason we determined the extent of a disorder of regional wall motion in two echocardiographic planes with reference to defined normal values. Analysis of interobserver and intraobserver variability showed that reproducible determinations of the circumferential extent of a disorder of regional wall motion and the ejection fraction are possible with an acceptable degree of certainty. There was a significant correlation between morphological determinations of the size of a perfusion defect in the left ventricle and the circumferential extent of a disorder of regional wall motions as demonstrated in the echocardiogram (r = 0.83). The regression curve (y = 4.26 + 0.95x) for determinations of the size of the perfusion defect approached the identity line with a standard error of estimation for the echocardiographic examination of 7.4%. Size of the zone of infarction was overestimated by an average of 8% with echocardiography (r = 0.81), with a standard error of estimation of 6.6% (y = -2.41 + 0.85x). There was no significant correlation between ejection fraction and size of the perfusion defect or the size of infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

[Long-term results following therapy with streptokinase in myocardial infarct]. / Langzeitergebnisse nach Therapie mit Streptokinase bei Myokardinfarkt.

Long term results of thrombolytic therapy in myocardial infarction are determined primarily by the effects of treatment in the acute phase. Out of a total of 370 patients undergoing recanalization therapy, 170 consecutive patients were examined over a period of one to three years (mean 1.5 years) by means of ECG, exercise testing, thallium myocardial scintigraphy, radionuclide ventriculography, coronary angiography and contrast ventriculography. Frequency of chest pain, left ventricular function, reinfarction rate and mortality were analyzed. The patient cohort was divided into three subgroups: 1. patients with successful PTCR who underwent PTCA or bypass graft surgery; 2. patients with successful PTCR who were managed medically without subsequent reinfarction; 3. patients with definitive occlusion or reinfarction. Mortality in the hospital phase (within 30 days) was 4.9% in patients undergoing successful recanalization procedures as compared to 12.3% for patients with definitive occlusion. Late mortality at 1.5 years was 12.3% and 16.2%, respectively. These figures are similar to those found in the literature. In-hospital mortality is clearly reduced by early recanalization within 200 minutes of occlusion, and there is a reduction in the ultimate extent of infarction as well as improvement in left ventricular function. In order to prevent reocclusion (in 10 to 20% of cases) and reinfarction additional interventions such as PTCA or bypass grafting should be employed as soon as possible in suitable cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracoronary thrombolysis: organizational prerequisites, technique, and results.

Reestablishing myocardial perfusion during evolving myocardial infarction may limit the ultimate extent of infarction if viable myocardial tissue is present when recanalization of the occluded vessel is achieved. This will result in improved left ventricular function and decreased mortality. In addition to their therapeutic benefits, recanalization procedures have contributed greatly to our knowledge of acute myocardial infarction. It has been demonstrated that myocardial infarction most often occurs after thrombotic occlusion of a coronary artery. This has settled a controversy that has preoccupied cardiologists for decades. Selective intracoronary administration of fibrinolytic agents is followed by recanalization in approximately 80% of cases. Therapeutic failures are attributable to occlusion caused by other factors, to inactivation of streptokinase by high antibody concentrations, and to insufficient concentrations of streptokinase at the thrombus as a result of unfavorable flow conditions.

[Idiopathic ventricular tachyarrhythmia. Spontaneous variability and effect of various antiarrhythmic agents]. / Idiopathische ventrikuläre Tachyarrhythmien. Spontanvariabilität und Wirkung verschiedener Antiarrhythmika.

20 patients with idiopathic complex ventricular arrhythmias received propafenone 450 mg/d, disopyramide 600 mg/d and metoprolol 100 mg/d. Before commencement of the 3-week treatment period the 95% normal range for spontaneous changes in ventricular extrasystoles (VES), as couplets and runs, were determined from three 24 h-ECG recordings in each patient under drug-free conditions. A drug effect was assumed when the rate of VES/24 h for the control period decreased by greater than or equal to 83.5% or increased by greater than or equal to 505% in the test period. The frequency dependent normal range for couplets varied between a decrease from 100% to 92% (greater than or equal to 16 to greater than or equal to 44/d) and an increase from 650% to 1000% (greater than or equal to 3 to greater than or equal to 38/d) and for runs between a decrease from 100% to 85% (greater than or equal to 6 to 32/d) and an increase from 600% to 1000% (greater than or equal to 1 to 14/d). A decrease in all rhythm disturbances under the action of the 3 drugs could be shown for the whole group (P less than 0.01). On the basis of the calculated normal range, ventricular extrasystoles in the patients decreased significantly by 26-37%, couplets by 13-33% and runs by 0-55% depending to the drug. A drug dependent arrhythmogenic effect occurred in 4 patients. A preference for one or other of the drugs could not be established statistically.

[Follow-up of late potentials and complex tachycardiac arrhythmias following myocardial infarct over a 2-year period]. / Verlaufsbeobachtungen von Spätpotentialen und komplexen tachykarden Rhythmusstörungen nach Myokardinfarkt über zwei Jahre.

50 patients (mean age 53.8 +/- 9.2 years) were studied at 1.5 to 2 months (U1), 12 months (U2) and 24 months (U3) after acute myocardial infarction. Late potentials were registered at the body surface using the signal-averaging technique and a digital Butterworth filter with high pass cut-off frequencies DC, 25, 50, 100 Hz and a low pass cut-off frequency 300 Hz, 18 db/octave, and a 24-hour ECG was recorded. All patients underwent coronary angiography at U1. Late potentials were found at least once during the observation period in 56% of patients, and 18% of patients demonstrated late potentials at all three examinations but up to 38% at one of the three examinations. Complex tachyarrhythmias (Lown class IV) were found at least once in 48% of patients and at all three examinations in 18% but up to 38% at one of the three examinations. Only four patients demonstrated late potentials and complex tachyarrhythmias at all three examination dates. In contrast, 36% of patients showed neither late potentials nor complex tachyarrhythmias at all three examinations. When late potentials and complex arrhythmias were present simultaneously, the former were most often detected at the cut-off frequencies DC, 25 to 300 Hz (p less than 0.05). The median of the duration of late potentials was significantly longer at U1 and U2 when complex arrhythmias were also present. There was a significant relation between late potentials and complex arrhythmias at U1 and U2 (p less than 0.01 and p less than 0.025) and between the latter and disorders of regional wall motion at all examination dates (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Detection of regional hypertrophy in hypertrophic cardiomyopathy with ECG triggered nuclear magnetic resonance tomography--comparison with hypertensive patients and persons with healthy hearts]. / Nachweis der regionalen Hypertrophie bei hypertrophischer Kardiomyopathie mit der EKG-getriggerten Kernspintomographie--Vergleich mit Hypertonikern und Herzgesunden.

Gated magnetic resonance tomography (MRT) was conducted in 40 patients (13 normal volunteers, 9 hypertensives and 18 patients with hypertrophic cardiomyopathy) using a 0.35 Tesla superconducting magnet. Multisectional spin echo imaging (35/400 msec) was obtained in coronal, transversal and sagittal planes. Myocardial wall thickness was measured in different segments and the three groups were compared to each other. 15/18 patients with hypertrophic cardiomyopathy (HCM) had asymmetrical regional thickening involving the septum and the anterior wall, in 8/15 the lateral wall was also hypertrophic. The distribution pattern in 3/15 patients with HCM was symmetric. Involvement of the right ventricle was found in 14/18 patients with HCM. There were significant differences (p less than 0.001) in wall thickness for the septal segment in all three groups and for the ratio septal to posterior wall between the HCM and the hypertensives and the normal volunteers. We conclude that MRT can differentiate HCM from hypertensives and normals, and is superior to echocardiographic imaging in the evaluation of the distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy.