Compromising bradycardia: management in the emergency department.

AIM OF THE STUDY: Bradycardia may represent a serious emergency. The need for temporary and permanent pacing is unknown. METHODS: We analysed a registry for the incidence, symptoms, presenting rhythm, underlying mechanism, management and outcome of patients presenting with compromising bradycardia to the emergency department of a university hospital retrospectively during a 10-year period. RESULTS: We identified 277 patients, 173 male (62%), median age 68 (IQR 58-78), median ventricular rate 33 min(-1) (IQR 30-40). The leading symptoms were syncope [94 (33%)], dizziness [61 (22%)], collapse [46 (17%)], angina [46 (17%)] and dyspnoea/heart failure [30 (11%)]. The initial ECG showed high grade AV block [134 (48%)], sinus bradycardia/AV block [46 (17%)], sinuatrial arrest [42 (15%)], bradycardic atrial fibrillation [39 (14%)] and pacemaker-failure [16 (6%)]. The underlying mechanisms were primary disturbance of cardiac automaticity and/or conduction [135 (49%)], adverse drug effect [58 (21%)], acute myocardial infarction [40 (14%)], pacemaker failure [16 (6%)], intoxication [16 (6%)] and electrolyte disorder [12 patients (4%)]. In 107 (39%) patients bed rest resolved the symptoms. Intravenous drugs to increase ventricular rate were given to 170 (61%) patients, 54 (20%) required additional temporary transvenous/transcutaneous pacing. Two severely intoxicated patients could be stabilised only by cardiopulmonary bypass. A permanent pacemaker was implanted in 137 patients (50%). Mortality was 5% at 30 days. CONCLUSION: In our cohort, about 20% of the patients presenting with compromising bradycardia required temporary emergency pacing for initial stabilisation, in 50% permanent pacing had to be established.

Natriuretic peptides and the prevalence of congestive heart failure in patients with pacemakers.

AIM: The aim of the study was to investigate the diagnostic potential of natriuretic cardiac peptide measurement in the context of left ventricular dysfunction and comorbidities in a pacemaker population. MATERIAL AND METHODS: Ninety-five consecutive patients with pacemakers were included in the study. All patients underwent echocardiography and were asked to complete the Minnesota Living with Heart Failure Questionnaire (MLHFQ). Brain natriuretic peptide (BNP), N-terminal proatrial natriuretic peptide (N-ANP) and atrial natriuretic peptide levels in plasma were measured. RESULTS: Twenty-six percent of patients had reduced systolic left ventricular function; only 16 patients had a history of congestive heart failure. BNP was abnormally elevated in 64%, N-BNP in 72% and N-ANP in 96% of patients. Both BNP (r = 0.30; P < 0.01) and N-ANP (r = 0.39; P < 0.0005) correlated with MLHFQ. The strongest correlation was found between N-ANP and the ejection fraction (r = 0.6; P < 0.0001). Patients were stratified in a high-risk group and a low risk-group according to their N-ANP (N-ANP > 5000 fmol L(-1); n = 63 and N-ANP < 5000 fmol L(-1), n = 32) and BNP levels (BNP > 400 pg mL(-1); n = 17 and BNP < 400 pg mL(-1), n = 78). N-ANP was correlated with hypertension (P < 0.003) and atrial fibrillation (P < 0.03), and BNP with mitral insufficiency (P < 0.002). CONCLUSIONS: Cardiac natriuretic peptides are markedly elevated in the majority of patients with pacemakers. The prognostic significance of BNP and N-ANP in left ventricular dysfunction warrants close follow-up schedules.

Diagnostic value of onset-recordings and marker annotations in dual chamber pacemaker stored electrograms.

AIMS: Stored electrograms (EGM) have recently been introduced into pacemaker therapy. New generation devices offer the possibility to store the onset of the EGM (several seconds preceding storage trigger) and marker annotations. The aim of the study was to evaluate whether the diagnostic capabilities of EGMs are improved by these new features. METHODS: We studied 65 patients (age 68+/-12 years, 41 male) implanted with a DDDR-system (PulsarMax II 1280; Guidant). During a 1-month period 319 EGMs have been recorded. EGM triggers were: Ventricular Tachycardia (VT), Non-Sustained VT (NSVT), Atrial Tachycardia Response (ATR), Pacemaker Mediated Tachycardia (PMT) and Sudden Bradycardia Response (SBR). First, each EGM was analysed with onset and markers blinded. EGMs were classified with respect to their trigger as confirmed, not-confirmed or false-positive. Analysis was then repeated with markers visible but without onset, and thereafter vice versa. Finally, EGMs were analysed with both features. It was noted whether the presence of marker annotations and/or onset-recording changed the initial classification of the stored EGMs. RESULTS: 169 EGMs were triggered by SBR, which can only be confirmed with onset recording. False positive EGMs (atrial undersensing) occurred in 12%. The remaining 150 EGMs were triggered by ATR (80%), NSVT (11%), VT (6%) and by PMT (3%). Without onset/markers 37 of these 150 EGMs (25%) could not be confirmed. With markers and onset 33/37 (89%) of these EGMs could now be classified as confirmed or false positive. These EGMs became diagnostic with onset alone in 24%, with markers alone in 24%, and with the combination of both in 41%. In 4 EGMs no definite diagnosis could be established. CONCLUSION: Stored electrograms provide direct insights into device function, thereby providing a validation of diagnostic data. The expanded recording of onset and markers results in markedly improved diagnostic capabilities - compared with conventional EGMs. These new features were necessary to interpret correctly 61% of all stored electrograms, without which a diagnosis would not have been possible. Both onset-recording and marker annotation are necessary for optimal analysis.

[Pacemaker dysfunction in the clinical practice]. / Schrittmacherdysfunktion in der klinischen Praxis.

Lead dysfunction is still the predominant cause of pacemaker dysfunction. Beyond lead dysfunction clinicians might encounter problems resulting from the surgical procedure of pacemaker implantation, from specific programmable pacemaker functions (e.g. undersensing of premature ventricular complexes when autosensing is activated) and from interference with electromagnetic fields. Electromagnetic interference between pacemakers and mobile phones has been demonstrated both in vitro and in vivo, but in daily life pacemaker patients can readily use mobile phones when certain security measures are taken into account. Electromagnetic interference between anti-theft devices and pacemakers can arise from situations where the pacemaker is in close proximity to the anti-theft device, but in daily life these interferences are rare. The electromagnetic fields generated during magnetic resonance imaging (MRI) are considerably stronger than those generated by mobile phones or anti-theft devices, therefore permanent pacemakers are still considered a contraindication for MRI, although several case reports have recently been published that reported on uneventful MRI procedures in pacemaker patients. The present review summarizes the current knowledge on the most frequent pacemaker dysfunctions and electromagnetic interferences that might be relevant in clinical practice.

Modified LDL decreases the binding of prostaglandin E2, I2, and E1 onto monocytes in patients with peripheral vascular disease.

Recent data suggest that various eicosanoids including prostaglandins play an important regulatory role in the development of atherosclerotic lesions. Peripheral blood monocytes have been implemented in early atherogenesis because they express receptors specific for modified LDL. In this study we investigated the binding of tritium prostaglandins E2 (3H-PGE2), E1 (3H-PGE1) and I2 (3H-PGI2) onto intact peripheral monocytes isolated from 20 patients (32-71 years) with manifested ischemic peripheral vascular disease stage II according to Fontaine and compared the results with those obtained in 16 healthy volunteers (21-68 years). In control subjects, Scatchard analyses of the binding data indicated a single class of high-affinity binding sites for 3H-PGE2 (maximal binding capacity [Bmax] = 11,400 +/- 3200 sites/cell; dissociation constant [Kd] = 1.3 +/- 0.5 nmol/L) and two classes of binding sites for 3H-PGE1 (Bmax1 = 11,200 +/- 4900 sites/cell, Kd1 = 1.5 +/- 0.5 nmol/L; Bmax2 = 47,800 +/- 6100 sites/cell, Kd2 = 12.8 +/- 5.9 nmol/L) as well as for 3H-PGI2 (Bmax1 = 10,100 +/- 3700 sites/cell, Kd1 = 1.7 +/- 0.7 nmol/L; Bmax2 = 81,200 +/- 5200 sites/cell, Kd2 = 14.2 +/- 6.5 nmol/L). In the patients, an absence of the higher-affinity binding class and significantly (P < .01) fewer lower-affinity binding sites were found for each ligand (PGE2: Bmax = 6600 +/- 3600 sites/cell, Kd = 12.1 +/- 3.2 nmol/L; PGI2: Bmax = 6400 +/- 3100 sites/cell, Kd = 22.1 +/- 8.3; PGE1: Bmax = 5300 +/- 1700 sites/ cell, Kd = 20.5 +/- 7.0 nmol/L). After incubation of monocytes with modified LDL (oxidized LDL or acetylated LDL), the binding of prostaglandins was significantly (P < .01 to P < .001) decreased, whereas native VLDL, LDL, and HDL did not interfere with prostaglandin binding. Prostaglandin-induced adenosine 3'-5' cyclic monophosphate (cAMP) formation by monocytes was significantly (P < .01) lower in patients (the concentrations causing 50% elevation of basal cAMP formation [ED50] were 3.8 +/- 2.4 nmol/L for PGE2, 6.3 +/- 3.5 nmol/L for PGE1, and 5.6 +/- 4.1 nmol/L for PGI2) than in the control subjects (ED50 was 1.6 +/- 1.2 nmol/L for PGE2, 4.8 +/- 2.5 nmol/L for PGE1, and 3.1 +/- 1.4 nmol/L for PGI2). After preincubation with modified LDL, the PG-induced cAMP production by monocytes was remarkably decreased in both patients and control subjects (P < .05). Our results suggest a direct effect of modified LDL on PGE2, PGE1, and PGI2 binding onto monocytes by reducing the number of cell surface-expressed receptors available. Modified LDL also reduces the sensitivity of monocytes to prostaglandins, which results in decreased cAMP production. The complex interactions between prostaglandins and lipoproteins may play an important role during atherogenesis.

Assessment of myocardial injury by serum tumour necrosis factor alpha measurements in acute myocardial infarction.

Clinical and experimental data have shown that after acute myocardial infarction there is a significant release of tumour necrosis factor alpha. Therefore, an attempt was made to correlate changes in serum tumour necrosis factor alpha concentrations with indices of infarct extent in patients with acute myocardial infarction. In 50 patients with acute myocardial infarction, blood samples for evaluation of tumour necrosis factor alpha and alpha-hydroxybutyrate-dehydrogenase were collected every 6 h until 120 h after admission. Infarct extent was estimated by clinical parameters such as the occurrence of heart failure and rhythm disturbances, by enzymatic methods such as cumulative release of alpha-hydroxybutyrate-dehydrogenase and imaging techniques, by late resting single photon emission tomography--201 thallium scintigraphy--using an extent score and by echocardiography using a wall motion index. The maximum change in serum tumour necrosis factor alpha after infarction (delta TNF) was calculated by subtracting tumour necrosis factor alpha concentration on admission from peak tumour necrosis factor alpha concentration. The average peak tumour necrosis factor alpha level was observed 84 h after admission (median: 12 pg.ml-1). Between the 72nd and the 96th h no significant changes in tumour necrosis factor alpha values were observed. Analysis of the data showed that larger delta (TNF) values were found to be associated significantly with signs of heart failure (P = 0.003), the presence of rhythm disturbances (P = 0.001), increased enzymatic infarct extent indicated by cumulative release of alpha-hydroxybutyrate-dehydrogenase (r = 0.74; P < 0.001), large myocardial perfusion defects measured with 201 thallium scintigraphy (r = 0.80; P < 0.001), and a considerable number of left ventricular wall motion abnormalities (r = 0.57; P < 0.001). In conclusion, delta (TNF) is a reliable method of assessing damage severity in the myocardium after acute myocardial infarction. As only two blood samples are necessary within 84 h, the method may be one of the more convenient for the assessment of infarct size in clinical practice.

[Antihypertensive therapy and coronary heart disease: significance of the effect of concomitant cardiovascular risk factors]. / Antihypertensive Therapie und koronare Herzkrankheit: die Bedeutung der Beeinflussung begleitender kardiovaskulärer Risikofaktoren.

Antihypertensive therapy as it was performed in the past has not provided the degree of protection against coronary heart disease as was originally predicted by epidemiologic evidence. An improvement of outcome of antihypertensive therapy can only be achieved if coronary risk is maximally reduced. Therefore, in treating hypertensive patients, one has to take care of a diligent search for the presence of other coexisting coronary risk factors, of a vigorous use of life-style modifications (nondrug therapy), and of a greater individual selectivity of antihypertensive agents for initial and chronic use, preferring those that may provide additional benefits for other coexisting coronary risks.

Isradipine inhibits mitotic and proliferative activity in the arterial wall.

The anti-mitotic (3H-thymidine uptake quantified using autoradiography) and anti-proliferative (counting of activated smooth muscle cells on semithin sections) effects of the dihydropyridine calcium channel blocker isradipine (0.3 mg/kg) have been assessed in a rabbit arterial stress model. Isradipine caused a significant drop in both mitotic and proliferative activity. These effects were more pronounced by pretreatment (6 hours before lesion induction with desoxycorticosterone) with isradipine as compared to posttreatment (6 hours after experimental lesioning). The benefit induced by isradipine was abolished by aspirin treatment. In-vitro vascular prostacyclin formation and cholesterol content were not affected. These findings suggest that the anti-atherosclerotic action of isradipine on mitotic activity and cellular proliferation is mediated by a cyclooxygenase product, most likely via enhanced local vascular PGI2-synthesis.

Etofibrate increases binding of low and high density lipoprotein to human platelets of patients with type II hyperlipoproteinemia.

Previous work suggested an influence of etofibrate, a diester of nicotinic acid and clofibric acid, on lipoprotein receptors. Besides its beneficial effects on plasma lipoprotein levels of decrease in total cholesterol, LDL-cholesterol and triglycerides and increase in HDL-cholesterol, etofibrate was shown to inhibit platelet function. In order to further evaluate platelet-lipoprotein interactions, the effects of etofibrate on plasma lipids and lipoproteins on the specific binding of normal [111In]LDL and [111In]HDL onto platelets as well as its effect on platelet function were evaluated in 8 patients affected by Type II hyperlipoproteinemia (HLP). In all patients binding was saturable and indicated high affinity binding sites capable of binding 927 +/- 233 ng protein of [111In]LDL/10(9) platelets (Kd 12 +/- 3 micrograms protein/ml) and 1496 +/- 435 ng protein of [111In]HDL/10(9) platelets (Kd 14 +/- 3 micrograms protein/ml). The capacity of native LDL (HDL) to displace bound [111In]LDL ([111In]HDL) by half (IC50) amounted to 22 +/- 9 micrograms protein/ml (26 +/- 8 micrograms protein/ml). Following a 6-week treatment period with etofibrate (500 mg twice daily), decrease in plasma total cholesterol, LDL-cholesterol and apolipoprotein (apo) B and increase in HDL-cholesterol and apo AI was correlated to a significant (P < 0.01) increase in LDL- as well as HDL-receptor binding. The platelet binding capacity increased to 1085 +/- 212 ng protein/10(9) platelets (Kd 8 +/- 3 micrograms protein/ml) for [111In]LDL and to 1867 +/- 266 ng protein/10(9) platelets for [111In]HDL (Kd 11 +/- 3 micrograms protein/ml). Platelet function studies demonstrated significantly (P < 0.01) reduced platelet aggregation in response to ADP and thromboxane formation after 6 weeks of etofibrate therapy. These findings in patients with HPL Type II indicate in vivo upregulation of specific [111In]LDL as well as [111In]HDL binding sites on human platelets associated with reduced platelet activation following etofibrate therapy.

[Gender-specific differences of risk factors of atherosclerosis. A study of 3,850 Vienna employees]. / Geschlechtsspezifische Unterschiede der Risikofaktoren der Atherosklerose. Eine Untersuchung an 3850 Wiener Berufstätigen.

Atherosclerosis is the most frequent cause of death in Austria as well as in the other western industrialized countries. Sex specific differences in the various age groups concerning relative myocardial infarction-mortality stimulated us to investigate the risk factors for atherosclerosis in 3850 employees. An extensive lipid status, liver and kidney function parameters were determined, the blood-pressure was measured, and a cardiovascular centered case history was examined. The mean cholesterol level and the LDL-cholesterol level in males were significantly higher than in females (cholesterol: males 223.8 +/- 56.8 mg/dl, females 208.2 +/- 43.3 mg/dl, LDL-cholesterol: male 151.9 +/- 55.1 mg/dl, female 132.2 +/- 40.1 mg/dl, p < 0.001). The mean HDL-cholesterol level in males were significantly lower than in females (males: 45.0 +/- 11.6 mg/dl, females 56.2 +/- 13.3 mg/dl, p < 0.001). No significant difference concerning smoking-behaviour could be determined between female and male participants in this cohort (33.0% of the males resp. 33.6% of the females stated that they smoked cigarettes). Hypercholesterolaemia and cigarette-smoking are the main risk factors for both sexes, however the situation of women-except for the 6th decade-is much better than that of men. Remarkable is the increasing number of female-smokers, especially at younger age.

The role of type-1 plasminogen activator inhibitor in failure of thrombolytic therapy with recombinant tissue plasminogen activator.

We investigated the possible role of type-1 plasminogen activator inhibitor (PAI-1) on success or failure of thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) in 10 responders and 10 non-responders with acute myocardial infarction and early initiation of therapy within 2 h of onset using the common infusion scheme (100 mg rt-PA over 3 h). We determined plasma levels of t-PA (activity and antigen) as well as PAI-1 (activity and antigen) in samples obtained before, during and after thrombolytic treatment and compared the course of each of those parameters between responders and non-responders to therapy. Success or failure of treatment was determined by a combination of noninvasive methods and proven by coronary angiography within 5 days of initiation of thrombolysis. Thirty, 60, 90, and 120 min after initiation of rt-PA infusion, specific t-PA activities in plasma of responders were 0.62, 0.63, 0.62, and 0.57 (IU/ng/ml), respectively, as compared to 0.42, 0.42, 0.40, and 0.32 (IU/ng/ml) in nonresponders (p < 0.001). Between 4 and 8 h after initiation of therapy, a time span known to be critical for thrombotic reocclusion, specific activities were still significantly elevated in responders as compared to non-responders (p < 0.01). PAI-1 activity levels, which were not detectable during rt-PA infusion in either group, recovered to pre-treatment values 2 h earlier in non-responders.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of cardiac output on peak t-PA plasma levels in patients receiving thrombolytic therapy with recombinant tissue-type plasminogen activator--correlation with patency rate.

We studied 35 consecutive patients with short onset of myocardial infarction who underwent thrombolytic therapy with rt-PA at a standard dosage regimen of 100 mg rt-PA total (10 mg given as a bolus followed by 50 mg, 20 mg and 20 mg per hour for 3 hours). These patients were monitored for t-PA antigen and t-PA activity and PAI-1 activity plasma levels during rt-PA infusion. Success or failure of thrombolytic therapy was evaluated by non-invasive criteria (early plasma creatine kinase peaks, early peak plasma myoglobin values, and electrocardiographic criteria) as well as by means of coronary angiography at the fourth day after thrombolytic treatment. In 24 (68.6%) of these patients a success of thrombolytic therapy could be established by these criteria, while 11 patients did not respond to thrombolytic therapy. Fifteen patients (14 responders and one non-responder) had to be excluded from the further evaluation because in these patients clinical laboratory data obtained upon admission before initiation of thrombolytic therapy were not complete. Therefore, 20 patients (10 responders and 10 non-responders) could further be analysed. The two groups of patients were not significantly different in body weight, body weight index, age, gender, liver or kidney functional parameters as determined before initiation of the thrombolytic therapy. Furthermore, PAI-1 plasma levels before initiation of thrombolytic therapy were not significantly different in the two groups, as were rt-PA dosage per body weight or body weight index.(ABSTRACT TRUNCATED AT 250 WORDS)

The diminished extracellular matrix production induced by isradipine, a calcium channel blocker, is completely abolished by cyclooxygenase inhibition.

Collagen and glycosaminoglycan synthesis are well known to be enhanced during early atherogenesis. In this experimental study the synthesis of collagen was determined using 14C proline incorporation, the glycosaminoglycan production by means of 35S-sulphate incorporation and subsequent quantification by means of autoradiography. Isradipine, a new calcium channel blocker of the dihydropyridine family at a dose of 0.3 mg/kg significantly (p less than 0.01) decreased the incorporation of both the radioactive precursors. This effect was abolished by a concomitant aspirin treatment, while aspirin alone did not exert any significant effect on the precursor incorporation. These data suggest that isradipine, which is known to stimulate PGI2 synthesis, may exert this antiatherosclerotic inhibitory action on extracellular matrix production via the endogenous liberation of PGI2.

Ticlopidine and platelet function in healthy volunteers.

The influence of a 4-weeks therapy with 500 mg ticlopidine daily on platelet function parameters was examined in 10 male healthy volunteers aged 20-33 years in order to extend the knowledge on the antiplatelet activity of this substance. Ticlopidine significantly (p less than 0.01) affected ex-vivo platelet aggregation induced by ADP and increased platelet sensitivity to the antiaggregatory action of PGI2. Generation of TXB2 from endogenous substrate during spontaneous clotting of blood (serum-TXB2), conversion of exogenous radiolabelled arachidonic acid into TXB2 and MDA-formation in isolated platelets were unaffected by the treatment. The TXB2-level in plasma of volunteers, however, was decreased, after administration of the drug. The diminished alpha-granule content liberation (beta-thromboglobulin: p less than 0.01; PDGF: p less than 0.01; PF4 not significant) indicates that ticlopidine induces a decrease in platelet activity. The beneficial effect on release reaction is not associated with a decrease in TXA2-formation. Our results demonstrate that ticlopidine inhibits platelet activity, especially the PDGF-release. These results confirm the value of this drug in the prevention of atherosclerosis and its thromboembolic complications.

Prostaglandin I2 and the nitric oxide donor molsidomine have synergistic effects on thromboresistance in man.

1. In vitro synergistic effects of nitric oxide and prostaglandin I2 (PGI2) have been shown. Consequently we examined any potentiating effect of the nitric oxide donor molsidomine on the reduction in thrombogenicity produced by PGI2 in patients with peripheral vascular disease. 2. Thirty-six patients all with peripheral and also coronary artery disease were randomly allocated to receive PGI2 5 ng kg-1 min-1 for 6 h daily, 5 days a week for 5 weeks, alone (12 patients), with molsidomine 12 mg daily (12 patients) or molsidomine 12 mg daily alone (12 patients). 3. The effect of each treatment regimen was measured in terms of femoral artery platelet uptake and platelet survival after autologous 111Indium-oxine labelling. Molsidomine alone had no effect on platelet uptake or survival but in combination with PGI2 it significantly potentiated the decreased platelet uptake and prolonged platelet survival observed with PGI2 alone.

Modification of platelet function by isosorbide dinitrate in patients with coronary artery disease.

The effect of a four weeks oral treatment with 100 mg isosorbide dinitrate (ISDN) daily on platelet function was evaluated in 40 patients (aged 40-65 years) with proven coronary artery disease. Isosorbide dinitrate decreased platelet reactivity to ADP (p less than 0.001), increased platelet sensitivity to PGI2 (p less than 0.01) while the production of TXB2 from exogenous arachidonic acid substrate and from endogenous substrate were both significantly reduced. Circulating platelet aggregates as measured by the Wu-test were markedly reduced (p less than 0.001) but there was little change in the plasma concentration of the platelet proteins beta-thromboglobulin and platelet factor 4. Overall, platelet activation correlated with smoking, hypertension and a family history of coronary artery disease. The reduced platelet activation seen during treatment with isosorbide dinitrate may contribute to the therapeutic benefit seen with this drug in patients with coronary artery disease.

In vivo quantification of cholesterol content in human carotid arteries by quantitative gamma-camera imaging after injection of autologous low density lipoproteins (LDL).

Low density lipoproteins (LDL) were isolated by immunoaffinity chromatography from 18 patients (31-70 years) suffering from primary hypercholesterolemia with angiographically proven atherosclerosis of either one or both carotid arteries. LDL were labeled with 123I (1 mCi/mg LDL) by the iodine monochloride method followed by purification with dialysis and immediately reinjected thereafter. Gamma-camera serial controls over carotid regions allowed visual detection of uptake of the radiocompound uptake in 12 out of the 18 patients. The lipid entry ratio (LER; counts over the vascular region/pixel as compared to the contralateral side after background subtraction) confirmed the visual findings. Whole body images performed until 20 h after reinjection showed 3 different kinetic types of LDL-influx into the vessel wall: decreasing (type I), increasing and then decreasing (type II) and continuously increasing (type III) with time. Four patients underwent endarterectomy within 2-7 weeks after gamma-camera imaging. Histological control revealed an extensive amount of "foam cells" in tissue samples derived during surgery and an absence of endothelial lining in samples belonging to patients with type II kinetics.

Isradipine improves platelet function in hypertensives.

The effect of treatment for eight weeks with isradipine 1.25 mg twice daily for 4 weeks and thereafter 2.5 mg twice daily for 4 weeks on ex vivo platelet function was investigated in 10 male hypertensive patients, aged 51 (6.1) y. Systolic and diastolic blood pressure, platelet aggregation in response to ADP, serum thromboxane B2 and beta-thromboglobulin levels were significantly decreased at rest before exercise ergometry, during exercise and at rest after exercise. The platelet count, platelet sensitivity and the plasma levels of 6-oxo-prostaglandin F1 alpha were not affected by isradipine. It is concluded that a compound that lowers blood pressure and inhibits platelet activation may be of clinical benefit in the routine treatment of hypertension.

Effects of isradipine on platelet function in hypertension at rest and during exercise.

The effects of eight weeks of treatment with isradipine (1.25 mg twice daily for four weeks, followed by 2.5 mg twice daily for four weeks) on ex vivo platelet function were investigated in ten male patients with hypertension. Systolic and diastolic blood pressures, platelet aggregation in response to adenosine diphosphate (ADP), serum thromboxane B2, and beta-thromboglobulin levels were significantly decreased (P less than .05) at rest before exercise ergometry, during exercise, and at rest after exercise. The platelet count and plasma levels of 6-oxo-prostaglandin F1 alpha (PGF1 alpha) were not affected by isradipine. It is concluded that treatment of hypertension with a compound that lowers blood pressure and inhibits platelet activation may be of clinical benefit when routinely applied in hypertensive patients.