Investigating two mobile just-in-time adaptive interventions to foster psychological resilience: research protocol of the DynaM-INT study.

BACKGROUND: Stress-related disorders such as anxiety and depression are highly prevalent and cause a tremendous burden for affected individuals and society. In order to improve prevention strategies, knowledge regarding resilience mechanisms and ways to boost them is highly needed. In the Dynamic Modelling of Resilience - interventional multicenter study (DynaM-INT), we will conduct a large-scale feasibility and preliminary efficacy test for two mobile- and wearable-based just-in-time adaptive interventions (JITAIs), designed to target putative resilience mechanisms. Deep participant phenotyping at baseline serves to identify individual predictors for intervention success in terms of target engagement and stress resilience. METHODS: DynaM-INT aims to recruit N = 250 healthy but vulnerable young adults in the transition phase between adolescence and adulthood (18-27 years) across five research sites (Berlin, Mainz, Nijmegen, Tel Aviv, and Warsaw). Participants are included if they report at least three negative burdensome past life events and show increased levels of internalizing symptoms while not being affected by any major mental disorder. Participants are characterized in a multimodal baseline phase, which includes neuropsychological tests, neuroimaging, bio-samples, sociodemographic and psychological questionnaires, a video-recorded interview, as well as ecological momentary assessments (EMA) and ecological physiological assessments (EPA). Subsequently, participants are randomly assigned to one of two ecological momentary interventions (EMIs), targeting either positive cognitive reappraisal or reward sensitivity. During the following intervention phase, participants' stress responses are tracked using EMA and EPA, and JITAIs are triggered if an individually calibrated stress threshold is crossed. In a three-month-long follow-up phase, parts of the baseline characterization phase are repeated. Throughout the entire study, stressor exposure and mental health are regularly monitored to calculate stressor reactivity as a proxy for outcome resilience. The online monitoring questionnaires and the repetition of the baseline questionnaires also serve to assess target engagement. DISCUSSION: The DynaM-INT study intends to advance the field of resilience research by feasibility-testing two new mechanistically targeted JITAIs that aim at increasing individual stress resilience and identifying predictors for successful intervention response. Determining these predictors is an important step toward future randomized controlled trials to establish the efficacy of these interventions.

Direct determination of hepatic extraction of verapamil in cardiac patients.

Hepatic extraction of verapamil was determined directly in cardiac patients undergoing diagnostic catheterization and receiving 10 mg verapamil intravenously or intra-arterially. The extraction curves of verapamil concentrations in blood from the ascending aorta and hepatic vein were similar to those reported after single intravenous doses of indocyanine green. The rectilinear fall in concentration lasted 10 to 15 min. Mean hepatic extraction of verapamil in four patients who received intravenous doses was 0.86 (range 0.84 to 0.89) and in four who received intra-arterial doses was 0.87 (range 0.83 to 0.89). These estimates are the same as those for hepatic first-pass extraction determined by indirect methods based on areas under plasma concentration-time curves and requiring calculation of apparent hepatic blood flow. The results were considered to be proof that the first-pass effect of verapamil after oral doses is attributable mainly, if not entirely, to hepatic elimination.

The effect of cyclosporine on electrically paced isolated rat cardiomyocytes.

The acute cardiotoxicity of cyclosporine was investigated in isolated cardiomyocytes from adult rats. In a first study, myocytes were incubated with CsA ranging from 1 to 10 micrograms/ml and paced by electrical-field stimulation. After 30 min of stimulation the number of surviving rod-shaped myocytes was significantly reduced at 2.5 micrograms/ml (77.9%) and 5 micrograms/ml CsA (64.2%) as compared with the drug vehicle methanol (88.8%, P less than 0.05) with a further decrease at 10 micrograms/ml CsA (30.1% vs. 81.2%, P less than 0.005). In a second study, with the use of digital image processing of fura-2 fluorescence, the mean intracellular free calcium concentration, integrated over 1 sec, of single myocytes in the presence of 5 micrograms/ml CsA, the solvent methanol, or pure Krebs Ringer Hepes buffer was measured. Starting 2 Hz field stimulation increased the intracellular free calcium concentration from 100.1 to 177.9 nM in buffer and from 145.7 to 200.6 nM calcium with methanol. In contrast, there was a 3-fold increase of the intracellular free calcium concentration with 5 micrograms/ml CsA from 128.8 to 376.1 nM calcium. The intracellular free calcium during electrical stimulation was significantly higher with CsA than with the solvent (376.1 nM vs. 200.6 nM, P less than 0.001). In a further study, myocytes were incubated with calcium ranging from 0.5 to 8 mM calcium in the presence of 5 micrograms/ml CsA or the solvent methanol and electrically stimulated. Here, with increasing extracellular calcium the number of rod-shaped myocytes decreased significantly with CsA as compared with the solvent (P less than 0.02). The data suggest that CsA exerts a dose-dependent toxic effect on isolated rat cardiomyocytes that depends on the extracellular calcium concentration. There is direct evidence that CsA increases the intracellular free calcium concentration in rat cardiomyocytes.

Chronic angiotensin-converting enzyme inhibition may improve sodium excretion in cardiac transplant hypertension.

Cyclosporine-associated hypertension (CAH) may be mediated in part by sodium and volume retention. To investigate this issue, we studied the effects of a calcium antagonist, nitrendipine (NIT, 10-20 mg b.i.d.), and a converting enzyme inhibitor, lisinopril (LIS, 10-20 mg o.d.), on blood pressure (office BP, 24 hr ambulatory BP), excretion of an acute sodium load (200 mmol/2 hr i.v.), glomerular filtration rate (insulin clearance), cumulative dopamine excretion, plasma atrial natriuretic peptide (ANP), and endothelin excretion in 8 patients with CAH after cardiac transplantation in a double-blind, randomized, crossover trial for 6 weeks. Five patients received a diuretic during the trial at a constant dose. Office diastolic BP (DBP) decreased significantly with LIS from 97 +/- 6 to 87 +/- 9 mmHg and with NIT from 96 +/- 7 to 92 +/- 12 mmHg. Ambulatory 24 hr DBP decreased significantly from 96 +/- 7 mmHg to 86 +/- 10 mmHg (LIS) and to 84 +/- 11 mmHg (NIT). Ambulatory DBP during the day was lowered significantly from 98 +/- 11 mmHg to 87 +/- 10 mmHg (LIS) and to 88 +/- 9 mmHg (NIT) and during the night from 95 +/- 9 mmHg to 86 +/- 8 mmHg (LIS) and to 79 +/- 7 mmHg (NIT). Cumulative sodium excretion 6 hr after an acute sodium load increased to 52 +/- 39 mmol (placebo), 96 +/- 44 mmol (LIS, P < 0.05 vs. placebo), and 71 +/- 34 mmol (NIT). Glomerular filtration rate, cumulative dopamine excretion, ANP, and endothelin excretion did not differ between either treatment group. We conclude, that: (1) both drugs were similar in lowering office BP and during the day, but NIT tended to be more effective during the night; and (2) cumulative sodium excretion during LIS was significantly increased compared with placebo. There was a similar trend during NIT also. Therefore, it is possible that chronic angiotensin-converting enzyme inhibition and possibly calcium antagonists might improve the sodium-retaining state in CAH independent of differences in blood pressure, ANP, dopamine, or renal function.

Relation of antianginal efficacy of nifedipine to degree of coronary arterial narrowing and to presence of coronary collateral vessels.

Thirty-six patients with chronic stable angina pectoris or with stable and vasospastic components of angina pectoris were classified by coronary arteriographic findings into 4 groups. Patients in group A had a single stenotic coronary artery; patients in groups B, C and D had occluded arteries, but these arteries had been collateralized to varying degrees, and an epicardial coronary steal phenomenon was possible. All patients underwent multiple exercise tests before and after randomized, double-blind, crossover treatment with 20 mg of nifedipine, 20 mg of isosorbide dinitrate, a combination of both, and placebo. Maximal and mean ST-segment depression, occurrence of angina pectoris and heart rate were evaluated. After nifedipine treatment, mean ischemic ST-segment depression was reduced 21% in group A (p less than 0.05), but was not significantly altered in the other groups (group B, 2% decrease; group C, 10% increase; group D, 3% decrease). However, isosorbide dinitrate reduced ST-segment depression significantly in all groups (group A, 29%, p less than 0.001; group B, 18%, p less than 0.01; group C, 19%, p less than 0.05; group D, 33%, p less than 0.05). The combination with nifedipine did not further improve the effect of isosorbide dinitrate. Maximal ST-segment depression and angina pectoris paralleled the changes in mean ST depression during the different medications. Heart rate at rest was not significantly changed after nifedipine treatment in any group, but increased significantly after isosorbide dinitrate treatment in groups B and C (group B, 12%, p less than 0.01; group C, 9%, p less than 0.05); heart rate during exercise did not differ significantly in any group or after any form of medication from placebo.

The Frankfurt experience in restenosis after coronary angioplasty.

Three hundred and thirty-three of 356 patients underwent angiographic follow-up from 1 to 18 months (mean 5.6 months) after percutaneous transluminal coronary angioplasty (PTCA). This is a reangiography rate of 94%. Recurrence rate after the first PTCA was 15% (n = 289). Restenosis rate was defined as an increase from immediate post-PTCA stenosis of more than 30%, or the loss of at least half of the initial gain in luminal diameter. Patients who needed a second angioplasty due to restenosis (n = 30) had a restenosis rate of 33%. Patients with angioplasty in the aortocoronary bypass (n = 14) had a restenosis rate of 45%. All patients were treated before, during and at least 4 to 6 months after the procedure with 60 to 100 mg of isosorbide dinitrate daily plus 160 to 360 mg of verapamil or 100 to 150 mg of gallopamil and 1.5 g of acetylsalicylic acid. In a second retrospective study 111 of 399 patients had the acetylsalicylic acid therapy discontinued or decreased. Forty-two of them developed restenosis (38%), whereas only 49 of 288 patients who continued to receive 1.5 g aspirin developed restenosis (17%). The restenosis rate was 32% in those who received the reduced dose of aspirin. Thus, a large dose of acetylsalicylic acid given before, during and 4 to 6 months after the procedure seems to be necessary to achieve a low rate of restenosis after PTCA.

Angiographic predictors of recurrence of restenosis after Wiktor stent implantation in native coronary arteries.

Intracoronary stenting has been proposed as an adjunct to balloon angioplasty to improve the immediate and long-term results. However, late luminal narrowing has been reported following the implantation of a variety of stents. One of the studies conducted with the Wiktor stent is a prospective registry designed to evaluate the feasibility, safety and efficacy of elective stent implantation in patients with documented restenosis of a native coronary artery. To identify angiographic variables predicting recurrence of restenosis, the angiograms of the first 91 patients with successful stent implantation and without clinical evidence of (sub)acute thrombotic stent occlusion were analyzed with the Computer Assisted Angiographic Analysis System using automated edge detection. The incidence of restenosis was 44% by patient and 45% by stent according to the 0.72 mm criterion, and 30% by patient and 29% by stent according to the 50% diameter stenosis criterion. The risk for restenosis for several angiographic variables was determined using an univariate analysis and is expressed as odds ratio with corresponding confidence interval. The only statistically significant predictor of restenosis was the relative gain when it exceeded 0.48 using the 0.72 mm criterion (odds ratio 2.7, 95% confidence interval 1.1-6.4). Furthermore, the relation between the relative gain (increase in minimal luminal diameter normalized to vessel size) as angiographic index of vessel wall injury and relative loss (decrease in minimal luminal diameter normalized to vessel size) as index of neointimal thickening was analyzed using a linear regression analysis. When using the categorical approach to address restenosis, there is an increased risk for recurrent restenosis when the relative gain exceeds 0.48. The continuous approach underscores this concept by indicating a weak but positive relation between the relative gain and relative loss.

Wiktor stent implantation in patients with restenosis following balloon angioplasty of a native coronary artery.

Intracoronary stenting has been introduced as an adjunct to balloon angioplasty aimed at overcoming its limitations, namely acute vessel closure and late restenosis. This study reports the first experience with the Wiktor stent implanted in the first 50 consecutive patients. All patients had restenosis of a native coronary artery lesion after prior balloon angioplasty. The target coronary artery was the left anterior descending artery in 26 patients, the circumflex artery in 7 patients and the right coronary artery in 17 patients. The implantation success rate was 98% (49 of 50 patients). There were no procedural deaths. Acute or subacute thrombotic stent occlusion occurred in 5 patients (10%). All 5 patients sustained a nonfatal acute myocardial infarction. Four of these patients underwent recanalization by means of balloon angioplasty; the remaining patient was referred for bypass surgery. A major bleeding complication occurred in 11 patients (22%): groin bleeding necessitating blood transfusion in 6, gastrointestinal bleeding in 3 and hematuria in 2. Repeat angiography was performed at a mean of 5.6 +/- 1.1 months in all but 1 patient undergoing implantation. Restenosis, defined by a reduction of greater than or equal to 0.72 mm in the minimal luminal diameter or a change in diameter stenosis from less than to greater than or equal to 50%, occurred in 20 (45%) and 13 (29%) patients, respectively. In this first experience, the easiness and high technical success rate of Wiktor stent implantation are overshadowed by a high incidence of subacute stent occlusion and bleeding complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Can the coronary atherosclerotic process be influenced by calcium antagonists?

Cell culture experiments and various animal models have shown that calcium antagonists can inhibit atheroma development. A number of antiatherosclerotic mechanisms have been proposed and the promising results of these in vitro and animal experiments prompted clinical trials. Retrospective analyses indicated that verapamil might retard disease progression and the development of new stenoses. Prospective clinical studies, however, have revealed no effect by calcium antagonists on pre-existing coronary stenoses (> or = 20%) and it is suggested that the study duration (2 to 3 years) may have been too short and that advanced stages of atheromatous disease are not influenced by calcium antagonists. Current data suggest that only early stages of coronary atheromatosis may be affected by treatment with calcium antagonists; however, optimum drug, dosage and suitable patients are yet to be defined.

Cyclosporine increases the intracellular free calcium concentration in electrically paced isolated rat cardiomyocytes.

The effect of cyclosporine on the mean cytoplasmic free calcium concentration in electrically paced single cardiomyocytes from adult rats was studied. Cardiac myocytes were paced by electrical field stimulation with either 2 or 3 Hz in the presence of 5 micrograms/ml cyclosporine or the solvent cremophor. Exposure to cyclosporine during 40 minutes of electrical pacing caused irreversible hypercontracture in most cells, only 22.1% +/- 1.2% (mean +/- SEM) remained rod-shaped versus 64.1% +/- 3.2% in the solvent (p = 0.01). The cytoplasmic free calcium concentration was measured by means of digital image processing of fura-2 fluorescence. Electrical field stimulation increased the cytoplasmic free calcium from 69.7 +/- 5.4 to 124.9 +/- 24.5 nmol/L Ca2+ in the presence of the solvent and from 84.2 +/- 25.4 to 250.1 +/- 55.9 nmol/L in the presence of cyclosporine (p = 0.036 versus solvent). The data provide direct evidence that cyclosporine enhances the cytoplasmic free calcium concentration in single paced rat cardiomyocytes. These findings may be of importance in the consideration of a possible cardiotoxicity of cyclosporine.

Ultrastructural calcium distribution and myocardial calcium content in human idiopathic dilated cardiomyopathy.

Myocardial calcium overload in chronic heart failure is still a debatable issue. The aim of this study was to investigate the myocardial calcium content and intracellular calcium distribution in end-stage dilated cardiomyopathy. The explanted hearts of 13 patients (9 male, 4 female, mean age 49 ± 12 years) undergoing heart transplantation because of end-stage dilated cardiomyopathy were examined. Samples were obtained from the right and left ventricular free wall and from the septum. Calcium and magnesium content were measured by atomic absorption spectrophotometry. Ultrastructural calcium distribution was examined in dilated cardiomyopathy using the phosphate-pyroantimonate method. Ultrastructural calcium distribution was also examined in left ventricular biopsies obtained from 3 patients (male, mean age 47 ± 3.6 years) with nonfailing hearts. The number of mitochondrial calcium precipitates was estimated morphometrically by a point counting method. Myocardial calcium and magnesium content in dilated cardiomyopathy did not differ significantly among the right and left ventricles and septum ranging from 8.5 to 10.8 mmol/kg dry weight. The phosphate-pyroantimonate method visualized calcium precipitates being confined to the sarcolemma, T-tubules, intercalated disks, and mitochondria in both nonfailing myocardium and dilated cardiomyopathy. Because mitochondria may act as buffers of cytoplasmic calcium, mitochondrial calcium precipitates served as a criterion for a possible cellular calcium overload. No differences in the amount of mitochondrial calcium deposits were observed between dilated cardiomyopathy and nonfailing hearts. The data suggest that there is no global myocardial calcium overload in human eng-stage dilated cardiomyopathy.

Calcium overload in human giant cell myocarditis.

Myocardial calcium overload was observed in a patient with giant cell myocarditis. The myocardial calcium content estimated by atomic absorption spectrophotometry amounted to 120 mEq/kg dry weight, and the von Kossa stain disclosed multiple foci with patchy calcifications of myocardial fibres. Cytochemical examination of the ultrastructural calcium localisation using the phosphate-pyroantimonate method showed considerable variation in the subcellular calcium distribution. In normal myocytes calcium precipitates were confined to the inner leaflet of the sarcolemma, T-tubules, intercalated disks, and sporadically to mitochondria. In contrast, extensive calcification of mitochondria and loss of sarcolemmal calcium was evident in necrotic myocytes. A number of grossly normal myocytes also showed an increase of calcium precipitates in slightly swollen mitochondria. These findings suggest that myocardial calcium overload in this case started in viable myocytes and was not merely a secondary phenomenon occurring after cell death.

Right ventricular volumes determined by computerized thermodilution in ischaemic heart disease: effect of exercise and nitroglycerin.

In 29 patients with stable ischaemic heart disease, right heart catheterization was performed to assess the effect of exercise and nitroglycerin on right ventricular volumes, which were determined by a new computerized thermodilution system. The coefficient of variation for the determination of right ventricular ejection fraction averaged 11.0 +/- 6.2% (mean +/- standard deviation) at rest and 14.6 +/- 8.1% during exercise. End-diastolic volume index increased from 90 (65-127) ml/m2 [median (range)] at rest to 101 (81-130) ml/m2 (P less than or equal to 0.0001) during exercise. Nitroglycerin reduced this parameter at rest to 77 (44-121) ml/m2 (P less than or equal to 0.05), without affecting exercise values. Resting right ventricular ejection fraction (55 [44-64]%) was diminished by both exercise (to 52 [39-62]%, P less than or equal to 0.05) and nitroglycerin (to 53 [40-65]%, P less than or equal to 0.05). Additionally, nitroglycerin reduced the exercise induced decrease of right ventricular ejection fraction from -3 (-20-10)% to -1 (-15-14)% (P less than or equal to 0.01). Nitroglycerin diminished the left-to-right interventricular end-diastolic pressure gradient, which was estimated from the difference between pulmonary capillary wedge pressure and right atrial pressure, at rest from 6 (1-17) mmHg to 5 (2-14) mmHg (P less than or equal to 0.05) and during exercise from 17 (6-31) mmHg to 14 (1-33) mmHg (P less than or equal to 0.001). It is concluded, that both exercise and nitroglycerin cause significant changes in right ventricular volumes.(ABSTRACT TRUNCATED AT 250 WORDS)

Restenosis is a common feature of the angiographic follow-up after balloon valvoplasty of calcified aortic stenoses.

Balloon dilatation of calcified aortic stenosis was attempted in 12 patients, 6 men and 6 women, aged 38-82 years. Two patients underwent emergency surgery because of myocardial injury or pericardial tamponade. One patient with severe depressed left ventricular function in whom the procedure was attempted in cardiogenic shock died during the procedure. One patient experienced severe aortic insufficiency after dilatation. The remaining pressure gradient was higher than 50 mm Hg in another patient. Seven dilatations were considered to be successful with a remaining pressure gradient below 50 mm Hg and a mean gradient reduction of 53 mm Hg. In one of these 7 patients, who suffered from severe heart failure, valvoplasty had been carried out to make aortic valve replacement possible. The operation was performed 2 weeks later without complications. Five of 6 patients treated medically after successful valvoplasty had restenosis within 3 to 12 months. One of them exhibited a good result at 3 months but severe restenosis after one year. It is concluded that balloon valvoplasty of calcified aortic stenosis cannot be considered an alternative to surgery. If, however, left ventricular function improves after successful valvoplasty, valve replacement will then carry less risk.

Beat-to-beat variation of heart rate in diabetic patients with autonomic neuropathy and in completely cardiac denervated patients following orthotopic heart transplantation.

Dysfunction of the vagal nerve, an early symptom in the development of autonomic neuropathy, can be assessed reliably by the beat-to-beat variation in heart rate. Patients after a cardiac transplantation are a unique model to investigate the beat-to-beat variation of a completely denervated heart. Heart rate and the beat-to-beat variation during normal and deep respiration were investigated in diabetic subjects with an autonomic neuropathy (n = 10), age and sex matched healthy controls (n = 10) and cardiac transplanted patients (n = 10). Further studies during pharmacological blockade of the parasympathetic nervous system with atropine were performed. In the denervated heart the coefficient of variation of the beat-to-beat interval was 0.38 +/- 0.02% during normal respiration, compared to 1.32 +/- 0.13% (P less than 0.0001) and 2.56 +/- 0.13% (P less than 0.0001) in the diabetic and control subjects, respectively. Administration of atropine (2 mg intravenously) decreased the coefficient of variation of the RR-interval to 0.73 +/- 0.09% in the diabetic patients (P less than 0.0005) and to 0.67 +/- 0.07% in the controls (P less than 0.0001), whereas the coefficient of variation remained unaffected in the cardiac denervated patients (0.39 +/- 0.02%). In the three groups an almost parallel increase of the RR-variation was observed during deep respiration at a rate of 6 breaths/min (from 0.38 +/- 0.02% to 1.99 +/- 0.38% in cardiac transplanted patients, P less than 0.0025; from 1.32 +/- 0.13% to 3.10 +/- 0.43% in diabetic patients, P less than 0.0025; from 2.56 +/- 0.13% to 5.42 +/- 0.94% in healthy controls, P less than 0.005). We conclude that a beat-to-beat variation of heart rate is present in the completely denervated heart. This RR-variation can not be influenced by a pharmacological blockade of the parasympathetic nervous system with atropine. The beat-to-beat variation increases during deep respiration not only in healthy controls but also in diabetic patients with autonomic neuropathy (partially denervated hearts) and cardiac transplanted patients (completely denervated hearts). This indicates an intracardiac mechanism in the modulation of heart rate.

Isolated rat cardiomyocytes as an experimental model for studying acute cardiotoxicity of cyclosporin A.

The acute cardiotoxicity of cyclosporin A was studied in isolated cardiac myocytes from adult rats. In an initial series of 7 animals, myocytes were incubated with concentrations of cyclosporin A ranging from 1 microgram/ml to 50 micrograms/ml. Shape changes of untreated cells, cells treated with cyclosporin A and cells treated with the solvent of cyclosporin A, Tween 80/ethanol, were evaluated. After 8 hours and 16 hours, respectively, of incubation 92 +/- 4.3% and 72 +/- 8.7% of the non-treated control cells were still rod-shaped. Cyclosporin A, however, in a concentration of 5 micrograms/ml decreased the number of rod-shaped cells (79 +/- 3.2% at 8 hours and 51 +/- 3.5% at 16 hours) in comparison to the solvent (94 +/- 3.5% at 8 hours and 76 +/- 5.8% at 16 hours, P less than 0.02). This effect became more pronounced with higher concentrations of cyclosporin A. On the other hand, Tween 80/ethanol alone in higher concentrations also led to a reduced number of rod-shaped cells. In a second series of 7 animals using Tween 80/ethanol and methanol as drug vehicles, myocytes were incubated for 16 hours with 15 micrograms/ml of cyclosporin A in a calcium containing medium (1 mM) or a calcium free medium (10(-4) M ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid). The number of remaining rod-shaped cells was higher in the calcium free medium as opposed to the medium containing calcium when the cells were exposed to cyclosporin A. It is concluded that in the applied model cyclosporin A at high concentrations has an acute cardiotoxic effect which in part appears to be calcium related.

Noninvasive assessment of left ventricular performance following transluminal coronary angioplasty.

We studied 36 patients with successful transluminal coronary angioplasty (group 1) noninvasively using exercise electrocardiography, exercise T1-201 myocardial scintigraphy and equilibrium radionuclide ventriculography before and 3-5 days after the procedure. Six patients who underwent aortocoronary-bypass surgery (group 2) and 10 patients with stable angina pectoris (group 3) served as controls. All patients had arteriographically documented coronary artery disease at least in one major coronary vessel (stenosis greater than or equal to 70%). In group 1, average coronary stenosis was 81.1 +/- 8.4% before dilatation and 44 +/- 13.7% after the procedure (P less than 0.001). Ischemia score in the exercise electrocardiography decreased from 2.4 +/- 2.7 before dilatation to 0.4 +/- 0.8 after the procedure (P less than 0.001). Myocardial perfusion in computerized T1-201 myocardial scintigraphy 5-10 min after exercise expressed as vitality index (the ratio of T1-201 uptake in the ischemic region to the region of maximal uptake in the same image analyzed carefully in the same view in 2 studies) increased from 72.9 +/- 8.4% before dilatation to 79.9 +/- 11.7% after the procedure (P less than 0.001). Ejection fraction at rest increased from 47.2 +/- 9.2% to 51.0 +/- 9.7% (P less than 0.001) and during exercise from 39.9 +/- 10.5% to 49.4 +/- 10.9% (P less than 0.001) before and after the procedure. In group 2, noninvasive studies showed a tendency to improvement after surgery. In group 3 no significant changes were noted. We conclude that transluminal coronary angioplasty improves both coronary perfusion to ischemic areas supplied by critical coronary artery stenoses and left ventricular function, especially during exercise, if luminal diameter is dilated by greater than 20%.

[Experience with a guidable catheter for angiography and bronchography (author's transl)]. / Erfahrungen mit einem lenkbaren Katheter in der Angiographie und Bronchographie

Despite certain disadvantages, depending partly on the design of the catheter and partly on other problems, a guidable catheter is, in many cases, the only means for achieving a successful angiographic examination. The guidable catheter is therefore a valuable addition to the equipment used for angiography.

[Results of combined myocardial scintigraphy and radionuclide ventriculography before and after transluminal coronary angioplasty of critical coronary artery stenoses]. / Ergebnisse der kombinierten Myokardszintigraphie und Radionuklidventrikulographie vor und nach transluminaler Koronarangioplastik kritischer Koronararterienstenosen.

This study compares exercise radionuclide ventriculography (RNVG) and exercise myocardial scintigraphy with 201Tl (MSC) both computed trisectorially. 137 patients before and after transluminal angioplasty (TCA) were investigated. While specificity equivalent was set at 90% for both methods (10% percentile of the controls [n = 29]) overall sensitivity for RNVG was 79% (n = 86) and for MSC 78% (n = 98). Sensitivity of RNVG for lesions of the posterior wall was lower than for the anterior wall: LAD stenoses 83% (n = 46), RCA stenoses 71% (n = 17), and LCX stenoses 63% (n = 8). Sensitivity of MSC presents only a slight difference between anterior and posterior wall lesions: LAD stenoses 78% (n = 51), RCA stenoses 73% (n = 22), RCX stenoses 100% (n = 8). Reproducibility of pathological findings before and after non-successful TCA and the determination of the stenosed vessel was slightly better with MSC than with RNVG. Functional improvement after a successful TCA is predictable by MSC, whereas RNVG documents the functional improvement.

[Multiparametric analysis using radionuclide ventriculography in the assessment of left ventricular function following heart transplantation]. / Multiparameteranalyse mittels Radionuklidventrikulographie in der Beurteilung der linksventrikulären Funktion nach Herztransplantation.

Left ventricular systolic and diastolic performance was evaluated by radionuclide angiography in 17 patients following cardiac transplantation and compared with normal persons. Both groups performed supine bicycle exercise during the investigation, the control group at 102 +/- 73 W and the transplanted patients at 61.2 +/- 15 W. The ejection fraction increased in the normal persons from 61 +/- 8 to 69 +/- 10% whereas in the transplanted patients it did not increase significantly. There were no relevant changes in systolic parameters during exercise in the transplant recipients. The changes in diastolic parameters were significantly smaller in transplant patients than in normals. After correction for heart rate-induced changes a significantly different time course of the systolic-diastolic sequence during the cardiac cycle became evident in the transplanted group at rest. During exercise the systolic-diastolic sequence during the cardiac cycle became similar in both groups. It is concluded that the reduced exercise capacity of patients in the late phase after cardiac transplantation is partially due to the absence of an EF increase and a limitation of diastolic reserve during exercise.