Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk.

OBJECTIVES: This study was performed to assess the efficacy of high dose intravenous heparin to treat mobile or protruding left ventricular thrombi as detected by serial echocardiography. BACKGROUND: The presence of mobile and protruding left ventricular thrombi greatly increases the risk of arterial embolization, yet optimal therapy, be it thrombolysis, anticoagulation or surgical removal, has not been defined. METHODS: Full dose heparin, 31,291 +/- 7,980 (mean +/- SD) IU/day, to prolong partial thromboplastin time to at least twice normal, was administered intravenously to 23 consecutive patients with 25 mobile and protruding thrombi. Patients were prospectively evaluated for hemorrhagic complications and embolic events during therapy. The presence or absence of thrombi and their size and characteristics were assessed by serial echocardiography. RESULTS: In all 23 patients left ventricular thrombi decreased in size, with disappearance of the high risk features. The duration of high dose heparin infusion was 7 to 22 days (mean 14 +/- 4). Thrombus size was reduced from 3.9 +/- 2.6 to 0.16 +/- 0.38 cm2, and thrombus disappeared entirely in 19 (83%) of 23 patients. No embolic events were detected during treatment, and the only complication was an upper gastrointestinal hemorrhage that was successfully treated medically. CONCLUSION: High dose intravenous heparin is a highly effective and safe treatment for completely resolving left ventricular thrombi with high risk features for embolization. Most such thrombi disappear completely within 1 to 3 weeks of this treatment without embolic or hemorrhagic complications.

A randomized study of coronary angioplasty compared with bypass surgery in patients with symptomatic multivessel coronary disease. German Angioplasty Bypass Surgery Investigation (GABI)

BACKGROUND: The standard treatment for patients with symptomatic multivessel coronary artery disease is coronary-artery bypass grafting (CABG). Percutaneous transluminal coronary angioplasty (PTCA) is widely used as an alternative approach to revascularization, but a systematic comparison of the two procedures is needed. We compared the outcomes in patients one year after complete revascularization with CABG or PTCA. METHODS: A total of 8981 patients with multivessel coronary disease were screened at eight clinical sites, and 359 patients were randomly assigned to undergo CABG (177 patients) or PTCA (182 patients). Enrollment required that complete revascularization of at least two major vessels supplying different myocardial regions be deemed clinically necessary and technically feasible. RESULTS: Among the patients in the CABG group, an average of 2.2 +/- 0.6 vessels were grafted, and among those in the PTCA group, 1.9 +/- 0.5 vessels were dilated. After CABG, hospitalization was longer (median, 19, as compared with 5 days for PTCA), and Q-wave myocardial infarction in relation to the procedure was more frequent (8.1 percent, as compared with 2.3 percent after PTCA; P = 0.022), whereas in-hospital mortality did not differ significantly between the two groups (2.5 percent in the CABG group and 1.1 percent in the PTCA group). At discharge 93 percent of the patients in the CABG group were free of angina, as compared with 82 percent of those in the PTCA group (P = 0.005). During the first year of follow-up, further interventions were necessary in 44 percent of the patients in the PTCA group (repeated PTCA in 23 percent, CABG in 18 percent, and both in 3 percent) but in only 6 percent of the patients in the CABG group (repeated CABG in 1 percent and PTCA in 5 percent; P < 0.001). Seventy-four percent of the patients in the CABG group and 71 percent of those in the PTCA group were free of angina one year after treatment. Exercise capacity improved similarly in both groups. However, 22 percent of the CABG group, as compared with only 12 percent of the PTCA group, did not require antianginal medication (P = 0.041). CONCLUSIONS: In selected patients with multivessel coronary disease, PTCA and CABG as initial treatments resulted in equivalent improvement in angina after one year. However, in order to achieve similar clinical outcomes, the patients treated with PTCA were more likely to require further interventions and antianginal drugs, whereas the patients treated with CABG were more likely to sustain an acute myocardial infarction at the time of the procedure.

Noninvasive estimation of regurgitant flow rate and volume in patients with mitral regurgitation by Doppler color mapping of accelerating flow field.

OBJECTIVES: This study was designed to examine the accuracy of proximal accelerating flow calculations in estimating regurgitant flow rate or volume in patients with different types of mitral valve disease. BACKGROUND: Flow acceleration proximal to a regurgitant orifice, observed with Doppler color flow mapping, is constituted by isovelocity surfaces centered at the orifice. By conservation of mass, the flow rate through each isovelocity surface equals the flow rate through the regurgitant orifice. METHODS: Forty-six adults with mitral regurgitation of angiographic grades I to IV were studied. The proximal accelerating flow rate (Q) was calculated by: Q = 2 pi r2.Vn, where pi r2 is the area of the hemisphere and Vn is the Nyquist velocity. Radius of the hemisphere (r) was measured from two-dimensional or M-mode Doppler color recording. From the M-mode color study, integration of accelerating flow rate throughout systole yielded stroke accelerating flow volume and mean flow rate. Mitral regurgitant flow rate and stroke regurgitant volume were measured by using a combination of pulsed wave Doppler and two-dimensional echocardiographic measurements of aortic forward flow and mitral inflow. RESULTS: The proximal accelerating flow region was observed in 42 of 46 patients. Maximal accelerating flow measured from either two-dimensional (372 +/- 389 ml/s) or M-mode (406 +/- 421 ml/s) Doppler color study tended to overestimate the mean regurgitant flow rate (306 +/- 253 ml/s, p < 0.05). Mean Doppler accelerating flow rate correlated well with mean regurgitant flow rate (r = 0.95, p < 0.001), although there was a tendency toward slight overestimation of mean regurgitant flow by mean accelerating flow in severe mitral regurgitation. However, there was no significant difference between the mean accelerating flow rate (318 +/- 304 ml/s) and the mean regurgitant flow rate (306 +/- 253 ml/s, p = NS) for all patients. A similar relation was found between accelerating flow stroke volume (78.27 +/- 62.72 ml) and regurgitant flow stroke volume (76.06 +/- 59.76 ml) (r = 0.95, p < 0.001). The etiology of mitral regurgitation did not appear to affect the relation between accelerating flow and regurgitant flow. CONCLUSIONS: Proximal accelerating flow rate calculated by the hemispheric model of the isovelocity surface was applicable and accurate in most patients with mitral regurgitation of a variety of causes. There was slight overestimation of regurgitant flow rate by accelerating flow rate when the regurgitant lesion was more severe.

Usefulness of transesophageal echocardiography in identifying small left ventricular apical thrombus.

OBJECTIVES: The aim of this study was to determine whether transesophageal echocardiography could clarify the nature of equivocal echodense structures in the left ventricular apical region frequently found on transthoracic echocardiography by directing the ultrasound beam from the left ventricular base to the apex and achieving better image quality. BACKGROUND: Transthoracic echocardiography often reveals an echogenic structure suggesting thrombus in the left ventricular apical region because of limited near-field resolution and echo vibration artifact in apical views. METHODS: Thirty-six patients with coronary artery disease or dilated cardiomyopathy who had apical wall motion abnormalities and equivocal transthoracic echodense structures were studied with transesophageal echocardiography using special manipulation of the transesophageal probe for adequate imaging of the apical region. Left ventricular thrombus was defined when echogenic structures with a clearly delineated margin adjacent to but distinct from the endocardium were observed in at least two different tomographic views in the four-chamber and left ventricular long-axis views during both systole and diastole. RESULTS: Left ventricular thrombus (mean size 1.3 +/- 0.7 cm2) was defined by transesophageal echocardiography in 19 (53%) of 36 patients with suspected thrombus on transthoracic echocardiography in the four-chamber or left ventricular long-axis view. Heavy trabeculation or extremely high echo reflection, or both, was observed in the apical region in 12 patients (33%). No extra structures in the apical region were found in five patients. In 19 patients with transesophageal echocardiographically defined thrombus, 6 patients (31%) experienced arterial embolic events before the transesophageal procedure. In contrast, none of 17 patients without transesophageal echocardiographically defined thrombi had systemic embolism (p < 0.03). CONCLUSIONS: 1) Transesophageal echocardiography is useful in identifying left ventricular apical thrombus in patients with unclear echogenic structures on transthoracic apical images; and 2) the high incidence of arterial embolism in patients with transesophageal echocardiographically detected left ventricular thrombus indicates the clinical importance of such thrombus.

Prevalence and mechanism of streptokinase-induced platelet stimulation. Effect of acetylsalicylic acid.

It was recently shown that streptokinase may induce clot formation in vivo by immunoglobulin G mediated platelet stimulation. We evaluated the in vitro effect of streptokinase on platelet function in 103 subjects, of whom 52 were < or = 30 years and 51 were > or = 50 years old. Although streptokinase inhibited platelet aggregation in the majority of cases, in nine the threshold concentration of ADP required to induce irreversible aggregation decreased with streptokinase (1 million Units. l-1) by 30% or more. This observation was confirmed in five of the nine by repeated measurements indicating reproducible streptokinase-induced platelet stimulation. Among the five, two were < or = 30, and three were > or = 50 years old. In none of the five subjects did the radio allergo sorbent test detect type E immunoglobulins directed against streptokinase in the serum. In contrast, in four of the five subjects, streptokinase-induced platelet hyperaggregability was suppressed by addition of goat antibodies against human immunoglobulin G, or F(ab')2-fragments of such antibodies. Acetylsalicylic acid did not prevent streptokinase-induced platelet stimulation, but in three of five cases, led to an increase in the control threshold concentration for ADP, so that after the decrease induced by streptokinase the threshold concentration for ADP was in the same range as before acetylsalicylic acid and streptokinase administration. Thus, streptokinase led to an inhibition of platelet aggregation in the majority of subjects evaluated. In a minority of five out of 103, however, streptokinase reproducibly caused platelet stimulation, presumably mediated by immunoglobulin G.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of dobutamine on pulmonary gas exchange in patients with severe heart failure.

Twenty patients (two female, 18 male, mean age 57 +/- 11 years) with severe heart failure NYHA IV (7 coronary artery disease, 13 congestive cardiomyopathy) were treated with 8.8 +/- 1.7 micrograms.kg-1 x min-1 of dobutamine. Pulmonary gas exchange was analysed by withdrawal of blood samples from a central venous catheter and a radial artery cannula. Dobutamine increased SvO2 from 58.7 +/- 11.2% to 72.2 +/- 6.3% (P = 0.0001) and decreased avDO2 from 7.7 +/- 2.45 Vol% to 4.97 +/- 1.34 Vol% (P = 0.0001). PaO2 and PaCO2 were not changed. Qs/Qt increased slightly from 9.1 +/- 8.3% to 11.3 +/- 6.4% (P = 0.035). Cardiac index increased by 51% (P = 0.0001), pulmonary capillary wedge pressure decreased by 28% (P = 0.0001). In patients with severe heart failure, dobutamine improved haemodynamics without detrimental effects on arterial oxygen concentration.

Intermittent infusion of dobutamine in the therapy of severe congestive heart failure--long-term effects and lack of tolerance.

Twenty patients with refractory heart failure NYHA class IV were randomly assigned to infusion therapy with 9.25 micrograms/kg/min dobutamine over 24 hours or placebo. Eight infusions over a 4-week period were performed in the hospital; between infusions breaks of 3 days were scheduled. A dose titration was performed before study during which dobutamine was infused at 2.5 micrograms/kg/min and increased by 2.5 micrograms/kg/min steps every 15 minutes up to a maximum dosage of 10 micrograms/kg/min. After dobutamine, exercise duration on the treadmill stress test increased from 177 +/- 110 seconds to 251 +/- 120 seconds (p less than 0.05). The heart-rate response to exercise increased (91 +/- 20 to 116 +/- 26 beats/min at baseline, 88 +/- 17 to 132 +/- 26 beats/min after therapy). Body weight decreased from 70.9 +/- 15.5 to 68.9 +/- 14.2 kg (p less than 0.03). On placebo, no significant changes were evident. Systolic time intervals and hemodynamic parameters showed only minor and not significant changes in both groups. No excess mortality emerged during intermittent dobutamine therapy. No clinical or hemodynamic signs of tolerance development were evident during control assessment 3 days after the last infusion. Intermittent therapy with dobutamine seems to be a promising concept in the management of refractory severe heart failure.

Diagnosis of thoracic aortic dissection. Magnetic resonance imaging versus transesophageal echocardiography.

BACKGROUND: Aortic dissection requires prompt and reliable diagnosis to reduce the high mortality. The purpose of this study was to assess the reliability of both ECG-triggered magnetic resonance imaging (MRI) and transesophageal two-dimensional echocardiography combined with color-coded Doppler flow imaging (TEE) for the diagnosis of thoracic aortic dissection and associated epiphenomena. METHODS AND RESULTS: Fifty-three consecutive patients with clinically suspected aortic dissection were subjected to a dual noninvasive imaging protocol in random order; imaging results were compared and validated against the independent morphological "gold standard" of intraoperative findings (n = 27), necropsy (n = 7), and/or contrast angiography (n = 53). No serious side effects were encountered with either imaging method. In contrast to a precursory screening transthoracic echogram, the sensitivities of both MRI and TEE were 100% for detecting a dissection of the thoracic aorta irrespective of its location. The specificity of TEE, however, was lower than the specificity of MRI for a dissection (TEE, 68.2% versus MRI, 100%; p less than 0.005), which resulted mainly from false-positive TEE findings confined to the ascending segment of the aorta (TEE, 78.8% versus MRI, 100%; p less than 0.01). In addition, MRI proved to be more sensitive than TEE in detecting the formation of thrombus in the false lumen of both the aortic arch (p less than 0.01) and the descending segment of the aorta (p less than 0.05). There were no discrepancies between the two imaging techniques in detecting the site of entry to a dissection, aortic regurgitation, or pericardial effusion. CONCLUSIONS: Both MRI and TEE are atraumatic, safe, and highly sensitive methods to identify and classify acute and subacute dissections of the entire thoracic aorta. TEE, however, is associated with lower specificity for lesions in the ascending aorta. These results may still favor TEE as a semi-invasive diagnostic procedure after a precursory screening transthoracic echogram in suspected aortic dissection, but they establish MRI as an excellent method to avoid false-positive findings. Anatomic mapping by MRI may emerge as the most comprehensive approach and morphological standard to guide surgical interventions.

Delayed coronary occlusion following primary successful angioplasty: management and outcome.

The treatment of delayed coronary occlusion after primary successful percutaneous transluminal coronary angioplasty (PTCA) is more difficult because surgical standby is often not available. The purpose of this study was to assess the therapeutic approaches and outcome of patients with delayed coronary occlusion from 30 to 180 minutes after successful PTCA. A delayed occlusion occurred in 18 (0.9%) (61 +/- 11 years; male n = 14, female n = 4) out of 2065 consecutive patients after PTCA. In 11 patients the dilated stenoses were located in the left descending artery, while seven patients had the stenosis in the right coronary artery. Twelve patients had unstable or postinfarction angina. The time interval between completion of PTCA and the onset of chest pain was 64 +/- 39 minutes. Immediate i.v. nitroglycerin resulted in no relief of the symptoms in any patient. One patient was operated upon at once, and one was given i.v. thrombolysis resulting in pain relief and reversal of ECG changes. The remaining 16 patients returned initially to the catheterization laboratory, where the occluded vessels were opened by mechanical recanalization. Three of them remained in stable condition. Due to impending reocclusion surgery was necessary in four patients and thrombolysis was performed in nine. After thrombolysis the vessel remained open in four patients. The other five needed bypass surgery on the day of PTCA. Myocardial infarction developed in nine patients (maximal CK 673 +/- 488 units/l). In conclusion, delayed occlusion after successful PTCA is a rare complication occurring primarily in patients with unstable angina. Mechanical recanalization opened the occluded vessel in most patients, and myocardial infarction was prevented in 50%.

[Improvement of chronic regionally impaired myocardial function immediately after coronary angioplasty]. / Verbesserung der chronisch regional eingeschränkten Myokardfunktion sofort nach Koronarangioplastie.

UNLABELLED: The effect of PTCA on chronically impaired, regional wall motion was studied in 40 patients with stable angina and stenoses in the left anterior descending artery. Left-ventricular angiograms were obtained before, 15 min after PTCA and, additionally, in eight patients 15 +/- 5 weeks after PTCA. Left-ventricular ejection fraction and regional myocardial function were assessed by the centerline method. Patients with no (n = 18) or non-Q-wave (n = 12) infarction were compared to patients with Q-wave infarction (n = 10). After PTCA, ejection fraction increased from 54 +/- 8% to 59 +/- 8% (p less than 0.05) and regional function improved significantly (maximal standard deviation before PTCA: 2.8 +/- 0.8; after PTCA: 1.9 +/- 0.9- segments below the first standard deviation before PTCA: 31 +/- 16; after PTCA: 19 +/- 17). The improvements were found in patients with no or non-Q-wave infarction. The benefit on regional function was unchanged at follow-up. CONCLUSIONS: PTCA reduced chronic regional myocardial dysfunction in 78% of the patients with stable angina within 15 min. Reversible myocardial dysfunction is most likely related to hibernating myocardium.

Effects of body constitution and age on maximum pacing rate of activity-modulated rate responsive pacemakers.

UNLABELLED: The pacing rate of activity-modulated pacemakers is triggered by vibrations running through the body. Whether the body constitution predicts maximum pacing rate and may facilitate rate response programming was studied in 16 patients with Activitrax pacemakers. Rate response parameters were programmed to a fixed setting in VVIR/VOOR mode (lower pacing rate 60 ppm, upper pacing rate 125-130 ppm, activity threshold medium/7). Body vibrations were induced by a treadmill exercise test with increasing speed. Maximum pacing rates were measured at the stage of symptom-limited tolerance. Exercise tests with a duration of 7.3 +/- 2.9 minutes resulted in a maximum pacing rate of 98 +/- 22 ppm ranging from 60-122 ppm. Maximum pacing rates did not differ between male (n = 10; 102 +/- 21 ppm) and female (n = 6; 92 +/- 24 ppm). Correlations between maximum pacing rates and body constitutional factors were not significant with r = -0.15 (weight), r = 0.39 (height), r = 0.07 (body surface area), and r = -0.27 (skin-fold thickness). The correlations with body mass index (r = -0.53) and age (r = -0.53) were initially significant, but not after Bonferroni-Simes-Hommel correction. The age-dependent relationship may be caused by the shorter exercise duration of older patients indicated by the correlation between exercise duration and maximum pacing rate (r = 0.77), as well as with age (r = -0.73). CONCLUSIONS: body constitution did not modify body vibrations and did not allow prediction of maximum pacing rates; therefore, it is no aid for the programming of rate response parameters.

[Results of emergency bypass operation following percutaneous transluminal coronary angioplasty]. / Ergebnisse der notfallmässigen Bypass-Operation nach perkutaner transluminaler Koronarangioplastie.

Between 1980 and 1988, percutaneous transluminal coronary angioplasty (PTCA) was performed in 1,514 patients. Fifty-five patients (3.6%) underwent emergency coronary bypass surgery because of an acute occlusion of the vessel or a dissection with sustained angina and signs of ischemia on the electrocardiogram. Twenty-five of these 55 patients had a myocardial infarction and 5 patients died, 3 perioperatively, 2 after hospital discharge. The degree of stenosis of the dilated vessel significantly influenced the incidence of infarction, while left ventricular ejection fraction prior to PTCA significantly influenced mortality. Patients who underwent surgery with an occluded vessel experienced myocardial infarction significantly more often (87%) than patients with a patent vessel (24%). The incidence of infarction was 27% when reperfusion of the vessel occluded during PTCA was achieved with a reperfusion catheter, repeated PTCA or intracoronary lysis. The patients' age, presence of unstable angina, left ventricular ejection fraction prior to PTCA, the dilated vessel, the extent of coronary artery disease, collateralization of the dilated vessel, and the time between the onset of the event necessitating bypass surgery and the beginning of extracorporeal circulation were found to have no influence on the incidence of infarction. Patients who died had a significantly lower ejection fraction before PTCA than survivors and all patients who died had experienced a large perioperative myocardial infarction.

Comparison of hormonal and haemodynamic changes after long-term oral therapy with pimobendan or enalapril--a double-blind randomized study.

Twenty-four patients (one female, 23 male) with mild to moderate heart failure were randomly and double-blindly assigned to an oral treatment with 5 mg enalapril twice daily or 5 mg pimobendan (UDCG 115) twice daily. After the first tablet intake, blood pressure and heart rate were measured for 6 h. Therapy continued over 6 months. Systolic arterial blood pressure dropped from 126 +/- 20 mmHg to 111 +/- 14 mmHg (P less than 0.05) after the first enalapril tablet and from 123 +/- 16 mmHg to 112 +/- 13 mmHg (P less than 0.05) after the first pimobendan tablet. After 6 months, no important changes in blood pressure were observed in the pimobendan group and only a minor decrease in the enalapril group. There was no significant change in heart rate either after the first dose or after long-term therapy with either medication. After 6 months, cardiac index increased from 2.73 +/- 0.75 l.min-1.m-2 to 3.38 +/- 0.69 l.min-1.m-2 (P less than 0.01) after pimobendam, but did not change after enalapril (2.95 +/- 0.75 l.min-1.m-2 to 2.96 +/- 0.89 l.min-1.m-2, NS). Pulmonary capillary wedge pressure decreased during pimobendan long-term therapy from 16 +/- 8 mmHg to 14 +/- 8 mmHg (NS) and during enalapril from 21 +/- 7 to 14 +/- 7 mmHg (P less than 0.01). Exercise capacity increased in the pimobendan group from 17.2 +/- 5.4 kJ to 23.0 +/- 9.6 kJ (P less than 0.05), and in the enalapril group from 20.4 +/- 11.9 kJ to 24.8 +/- 18.5 kJ (NS) during long-term therapy over 6 months. Plasma renin activity increased from 0.96 to 3.6 ng.ml-1.h-1 (P less than 0.05) during enalapril long-term therapy, but remained unchanged (1.38 vs. 1.32 ng.ml-1.h-1, NS) during pimobendan. The new inotrope, pimobendan, exerted favourable long-term effects without haemodynamic or humoral signs of tolerance development.

[The effect of step rate and muscle force on the rate response of activity-modulated cardiac pacemaker]. / Einfluss der Schrittfrequenz und Muskelkraft auf die Stimulationsfrequenz aktivitätsgesteuerter Herzschrittmacher.

Programming of activity-modulated pacemakers allows an individual adaptation of rate response. In 26 pacemaker patients (Activitrax n = 16; Synergyst n = 10; Medtronic) it was tested whether rate-response parameters can already be programmed under consideration of patient's characteristics. At a fixed rate-response setting (VVIR/VOOR mode, pacing rate range: 60-130 ppm, MEDIUM/7) four treadmill exercise tests were performed: three step-rate controlled tests with 40, 80, and 120 steps/min and a symptom-limited exercise test with 1 km/h initial speed and 1 km/h speed increments every second minute. Maximal pacing rates at 80 steps/min (72 +/- 14 ppm) and 120 steps/min (90 +/- 6 ppm) were higher than at 40 steps/min (63 +/- 6 ppm). Forced steps with a step rate of 40/min resulted in a higher pacing rate compared to normal steps. At symptom-limited exercise, maximum pacing rates increased to 102 +/- 19 ppm with a range from 60 ppm to 124 ppm. Positive correlations were found between maximum step rate and maximum pacing rate (r = 0.55), between exercise duration and maximum pacing rate (r = 0.70), and between exercise duration and maximum step rate (r = 0.78). Patients with an exercise tolerance up to 5 km/h achieved pacing rates from 91 and 124 ppm, but patients with restricted exercise tolerance had lower maximum pacing rates due to their lower maximum step frequencies. Step rate and body force are important movements in the generation of body vibrations.

Age, cardiovascular risk factors and coronary heart disease as determinants of platelet function in men. A multivariate approach.

Older age, the cardiovascular risk factors and arteriosclerosis have been reported to be associated with stimulated platelet function. To evaluate the relative importance of these factors in determining platelet function, a cross-sectional multivariate study in 191 men, 113 healthy subjects and 78 patients with angiographically documented coronary heart disease, was performed. In healthy subjects, stepwise multiple linear regression identified age to be a major determinant of platelet aggregability. After induction with both ADP and collagen the platelet aggregatory response markedly increased with age. In the patients, platelet function was not age dependent. In multivariate analysis of variance, neither smoking status nor hypercholesterolemia (greater than or equal to 240 mg/dl) were determinants of platelet function in either group. An increase in systolic blood pressure was associated with slightly more inhibited ADP induced aggregation in both healthy subjects and patients with coronary heart disease. In patients compared to healthy subjects, aggregation after induction with ADP and collagen was markedly enhanced and the in vitro formation of thromboxane after collagen stimulation increased. Thus, by multivariate analysis, age and the presence or absence of coronary heart disease were found to be major determinants of platelet function. In contrast, the cardiovascular risk factors smoking, hypercholesterolemia and hypertension were associated with only minor or no alterations of platelet function.

[Low-dose fish oil in primary hypertriglyceridemia. A randomized placebo-controlled study]. / Niedrig dosiertes Fischöl bei primärer Hypertriglyzeridämie. Eine randomisierte Placebo-kontrollierte Studie.

In a double-blind, randomized, placebo-controlled trial, we prospectively investigated the effects of two low doses of fish oil (10.5 and 5.25 g daily) in capsule form in patients with primary hypertriglyceridemia. During a 6 weeks' therapy with 10.5 g fish oil, serum triglycerides decreased by a mean of 38% from 578 +/- 167 to 358 +/- 66 mg/dl (p less than 0.05). With 5.25 g daily, triglyceride levels fell by 20% from 538 +/- 100 to 431 +/- 64 mg/dl (n.s.). With placebo, triglycerides increased by 8% from 835 +/- 176 to 900 +/- 228 mg/dl (n.s.). Total and HLD-cholesterol levels remained uninfluenced in all groups. Serum alkaline phosphatase decreased by a mean of 12% from 86 +/- 7 to 76 +/- 6 units/l in the patients treated with 10.5 g fish oil (p less than 0.01). Platelet aggregation after induction with collagen was slightly, but significantly inhibited in the patients treated with the higher dose of fish oil. Thus, in patients with primary hypertriglyceridemia, fish oil at a daily dose of 10.5, but not at 5.25 g, led to a significant reduction of serum triglyceride levels and to an inhibition of platelet aggregation.

[Loading-induced ST-interval elevations in the case of normal coronary arteries. The angiographic demonstration of loading-induced coronary artery spasm]. / Belastungsinduzierte ST-Strecken-Hebungen bei normalen Koronararterien. Angiographischer Nachweis eines belastungsinduzierten Koronararterienspasmus.

In a 60-year-old man with exercise-dependent anginal symptoms, reversible ST segment elevations of maximally 0.8 mV occurred in the anterior chest leads during ergometric exercise at 75 W. Angiography excluded coronary artery stenoses. To demonstrate whether he had exercise-dependent vasospastic angina, angiography was performed during bicycle ergometry. At 75 W the typical symptoms recurred, accompanied by ST elevations in the ECG. At the same time, spasm in the region of the anterior interventricular branch was demonstrated angiographically; it disappeared at once after intracoronary injection of 200 micrograms nitroglycerin. The patient subsequently remained free of symptoms while taking isosorbide dinitrate (120 mg daily) and nifedipine (80 mg daily).

[Diagnosis of suspected acute myocardial infarct in acute regional myocarditis]. / Verdachtsdiagnose akuter Myokardinfarkt bei akuter regionaler Myokarditis.

We report on 4 patients in whom acute myocardial infarction was suspected due to acute onset of chest pain and elevation of the ST-segment. Furthermore in 2 patients the echocardiography revealed regional abnormal wall motion on admission, the others later. Coronary angiography showed normal coronary arteries in all cases. The left ventricular angiogram namely demonstrated regional abnormal wall motion. 2 patients developed a slight increase of the creatine phosphokinase including the CK-MB. Only one patient mentioned a grippal infectious disease 6 weeks before. During the hospital time all patients presented one of the inflammatory signs. A demonstration of the infectious agent was not possible in any of the cases. The endomyocardial biopsy was positive in two cases, and slightly positive in one case. Sometimes regional myocarditis might imitate an acute myocardial infarction. Both, the exact anamnesis and coronary angiography are necessary. The performance of an endomyocardial biopsy is desirable.