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Background: Impaired renal function is associated with increased mortality among heart failure patients. Although a significant proportion of heart transplant (HTx) recipients have reduced renal function at 1 year post-HTx, no previous study has evaluated the associated risk for both all-cause and cardiac mortality. Hence, we assessed the relationship between glomerular filtration rate (GFR) at 1 year post-HTx and all-cause and cardiac mortality and development of cardiac allograft vasculopathy (CAV)., Methods: We evaluated 381 patients with a minimum survival of 1 year post-HTx and the Modification of Diet in Renal Disease Study formula was used to calculate estimated GFR. Mortality and angiographic CAV were defined as separate endpoints, and median follow-up was 7.4 and 4.0 years, respectively., Results: During the follow-up period, 122 patients died and 154 patients developed CAV. Reduced GFR pre-HTx was not a risk factor for either endpoint. Overall, 193 (51%) patients had GFR <60 ml/min/1.73 m at one year post-HTx and this was an independent predictor of all-cause mortality with an adjusted hazard ratio of 1.7 (P=0.01) for a GFR between 30-60 and 3.2 (P=0.006) for GFR <30 ml/min/1.73 m. GFR <60 ml/min/1.73 m at 1 year post-HTx was also associated with a higher risk of cardiac mortality (HR=1.9; P=0.04) but did not predict the development of CAV., Conclusions: Renal impairment is evident in a majority of HTx recipients at 1 year post-HTx. It is an important risk factor for both all-cause and cardiac mortality but does not predict the development of angiographic CAV.

Background: Neurohormones may influence vascular tone both during and after exercise. Neuropeptide Y (NPY), which is costored and released with norepinephrine (NE) during sympathetic activity, is a potent vasoconstrictor with a relatively long half-life. We therefore examined its possible association with the ischemic response to exercise in patients with coronary artery disease., Methods and Results: Twenty-nine male patients with effort-induced angina pectoris underwent a symptom-limited exercise test. In addition to conventional ST-segment analysis, we examined ischemia on the basis of heart rate (HR)-adjusted ST-segment changes through calculation of the ST/HR slope during the final 4 minutes of exercise and of the ST/HR recovery loop after exercise. Blood samples were taken before, during, and after exercise for an analysis of several neurohormones. Mean ST-segment depression was -223+/-20.2 microV (P:<0.0001) just before the termination of exercise, followed by a gradual normalization, but it remained significant after 10 minutes (-49+/-8.9 microV, P:<0.0001). At the end of exercise, the ST/HR slope, which reflects myocardial ischemia, was -6.0+/-0.77 microV/HR. In most patients, ST-segment levels at a given HR were lower during recovery than during exercise, here referred to as ST "deficit." Exercise increased the plasma levels of NPY, NE, epinephrine, and N-terminal proatrial natriuretic peptide, but big endothelin remained unchanged. Although NE and epinephrine peaked at maximal exercise, the highest levels of NPY and N-terminal proatrial natriuretic peptide were observed 4 minutes after exercise. The maximal increase in the NPY correlated significantly with ST-segment depression at 3 minutes after exercise (r=-0.61, P:= 0.0005), the ST deficit at the corresponding time point (r=-0.66, P:= 0.0001), and the duration of ST-segment depression after exercise (r= 0.42, P:=0.02). In contrast, no such correlations were found for NE., Conclusions: The present study has for the first time demonstrated a correlation between plasma NPY levels and the degree and duration of ST-segment depression after exercise in patients with coronary artery disease, which suggests that NPY may contribute to myocardial ischemia in these patients.

Objectives: Our intent was to investigate the effect of the dihydropyridine calcium channel blocker amlodipine on restenosis and clinical outcome in patients undergoing percutaneous transluminal coronary angioplasty (PTCA)., Background: Amlodipine has sustained vasodilatory effects and relieves coronary spasm, which may reduce luminal loss and clinical complications after PTCA., Methods: In a prospective, double-blind design, 635 patients were randomized to 10 mg of amlodipine or placebo. Pretreatment with the study drug started two weeks before PTCA and continued until four months after PTCA. The primary angiographic end point was loss in minimal lumen diameter (MLD) from post-PTCA to follow-up, as assessed by quantitative coronary angiography (QCA). Clinical end points were death, myocardial infarction, coronary artery bypass graft surgery and repeat PTCA (major adverse clinical events)., Results: Angioplasty was performed in 585 patients (92.1%); 91 patients (15.6%) had coronary stents implanted. Follow-up angiography suitable for QCA analysis was done in 236 patients in the amlodipine group and 215 patients in the placebo group (per-protocol group). The mean loss in MLD was 0.30 +/- 0.45 mm in the amlodipine group versus 0.29 +/- 0.49 mm in the placebo group (p = 0.84). The need for repeat PTCA was significantly lower in the amlodipine versus the placebo group (10 [3.1%] vs. 23 patients [7.3%], p = 0.02, relative risk ratio [RR]: 0.45, 95% confidence interval [CI]: 0.22 to 0.91), and the composite incidence of clinical events (30 [9.4%] vs. 46 patients (14.5%), p = 0.049, RR: 0.65, CI: 0.43 to 0.99) within the four months follow-up period (intention-to-treat analysis)., Conclusions: Amlodipine therapy starting two weeks before PTCA did not reduce luminal loss, but the incidence of repeat PTCA and the composite major adverse clinical events were significantly reduced during the four-month follow-up period after PTCA with amlodipine as compared with placebo.

Background: The effect of percutaneous transluminal coronary angioplasty (PTCA) on physiologic measurements has previously been shown, but the relation between physiologic response and degree of change in coronary luminal diameter is not known. We studied the relation between exercise capacity and minimal luminal diameter before and after PTCA. We also explored the usefulness of measurement of attenuation in exercise capacity after PTCA to predict the likelihood of restenosis., Methods: Bicycle exercise testing was performed 2 weeks before and 2 and 20 weeks after PTCA in 395 consecutively enrolled patients. Angiograms obtained before and after PTCA and 20 weeks afterward were analyzed by quantitative coronary angiography. Restenosis was defined as both angiographic (>/=50% diameter stenosis at follow-up angiography) and clinical (target-vessel revascularization), after successful PTCA. Exercise capacity was defined as the cumulative work performed divided by body weight (watt x minutes x kilograms(-1))., Results: Exercise capacity increased 43% (P <.0001) from before PTCA to 2 weeks after PTCA (early increase) and decreased 4% (P =.01) from 2 to 20 weeks after PTCA (late decrease). The gain in minimal luminal diameter (Minimal luminal diameter after - Minimal luminal diameter before) was 0.92 +/- 0.46 mm. The loss in minimal luminal diameter (Minimal luminal diameter after PTCA - Minimal luminal diameter at follow-up examination) was 0.27 +/- 0.42 mm. Exercise capacity and minimal luminal diameter measured before PTCA were positively correlated (coefficient 3.3; R = 0.12; P =.01). Gain in minimal luminal diameter correlated with the early increase in exercise capacity (coefficient -3.8; R = 0.23; P <.0001). Loss in minimal luminal diameter correlated with the late decrease in exercise capacity (coefficient 3.3; R = 0.20; P <.0001). Multivariate logistic regression analysis revealed that the late decrease in exercise capacity was independently predictive of both angiographically (odds ratio 1.13; P <.0001) and clinically (odds ratio 1.12; P <.0001) defined restenosis., Conclusions: The results demonstrated a linear relation between the severity of coronary stenosis and exercise capacity measured before PTCA. The degree of coronary luminal enlargement achieved with angioplasty and the luminal reduction that occurred between PTCA and follow-up evaluation correlated with increases and decreases in exercise capacity. Attenuation in exercise capacity was found to be a strong predictor of restenosis.

Transplant coronary artery disease (Tx-CAD) is the main determinant of long-term prognosis after heart transplantation. Immunologic processes may play a central role in the development of Tx-CAD, but the pathogenesis has not been fully clarified. We examined plasma levels of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL)-1beta and IL-6, and the CC-chemokine macrophage chemoattractant protein-1 (MCP-1) in 62 cardiac allograft recipients undergoing yearly heart catherization with coronary angiography for evaluation of graft disease. In this cross-sectional study, we found significantly increased levels of IL-1beta, IL-6, TNF-alpha, and MCP-1 compared with healthy controls even several years (median 7 years) after transplantation in periods with no intercurrent illness. Although no significant differences were found in plasma levels of IL-1beta and TNF-alpha between patients with (n = 25) and without (n = 37) Tx-CAD, the Tx-CAD group had significantly increased levels of IL-6 and MCP-1 compared with both controls and transplant recipients without Tx-CAD. Increased IL-6 levels compared with controls were found only in patients with Tx-CAD. Finally, while there was no significant relation between Tx-CAD and altered lipid status, the combination of high plasma concentrations of IL-6 or MCP-1 and high low-density lipoprotein cholesterol was strongly associated with increased occurrence of Tx-CAD. These findings indicate that cardiac allograft recipients have a persistent immune activation long term after transplantation. This activation, as particularly reflected in increased MCP-1 and IL-6 levels, may be related to the development of Tx-CAD.

Aims: Lipoproteins and lipids, especially lipoprotein(a), have been studied as risk factors for restenosis after coronary angioplasty with conflicting results. We investigated the association between serum levels of lipoprotein(a) apolipoprotein A-1, apolipoprotein B-100, total-cholesterol, high density lipoprotein-cholesterol, triglycerides, and coronary luminal loss and restenosis after angioplasty., Methods: The lipoproteins and lipids were measured in 305 consecutive patients who underwent successful angioplasty and reangiography 20+/-3 weeks after angioplasty. Single-vessel dilatation was performed in 251 patients. Luminal loss was defined as minimal luminal diameter post-angioplasty minus minimal luminal diameter at follow-up, divided by the interpolated reference diameter of the vessel. Restenosis was defined according to three dichotomous categorical criteria: (1) >50% diameter stenosis at follow-up (2) loss of >50% of the gain achieved by angioplasty, (3) the need for target vessel revascularization., Results: There was no significant association between the serum levels of lipoproteins and lipids and luminal loss. Univariate analysis did not show any significant difference in the serum levels of any of the lipoproteins and lipids between the restenosis and no-restenosis groups. Multivariate analysis revealed that only the angiographic variables (luminal gain and post-angioplasty minimal luminal diameter) were associated with luminal loss and restenosis after angioplasty., Conclusion: Lipoproteins and lipids were neither associated with luminal loss nor independent risk factors for restenosis after angioplasty.

Purpose: To describe changes in the coronary artery following heart transplantation (HTx) in patients who survived for 1 year or more., Material and Methods: Yearly ventriculography and coronary angiography were performed in 171 out of 172 patients aged over 12 years who survived HTx in Norway for 1 year or more after the first operation in 1983. Mean follow-up was 5.2 years +/- 2.8, range 1-12., Results: Altogether 31 patients died in the follow-up period, 8 (26%) of them from coronary artery disease (CAD). Angiographic changes included coronary artery stenoses, diffuse changes with ectatic and narrowed segments of the major coronary vessels, peripheral changes with occlusions and tapering of the small vessels, and reduction in the left ventricular ejection fraction (EF). Significant stenosis developed in 43 patients and 19 of these developed an occlusion of one of the major coronary artery branches. The coronary arteries were without significant stenosis in 97% of the surviving 141 patients at 1 year after HTx and in 82% at 5 years. Completely normal findings were seen in 81% after 1 year and in 44% after 5 years. Progression to significant stenosis and occlusion was rapid once changes first appeared., Conclusion: CAD contributed to a significant number of deaths. The stenoses could develop at any time after transplantation and usually progressed rapidly once the first changes appeared.

The use of minimally invasive direct coronary artery bypass grafting without cardiopulmonary bypass in combination with intraoperative percutaneous transluminal coronary angioplasty for myocardial revascularization in a heart transplant recipient is reported.

Aims: To study the impact of smoking on the change in exercise capacity in patients treated with coronary angioplasty., Methods: Three hundred and sixty-eight men below 70 years of age eligible for percutaneous transluminal coronary angioplasty without previous coronary interventions were consecutively enrolled. Of the 334 patients (90.8%) who completed the study 77 (23.1%) were current smokers. Exercise tests were performed before percutaneous transluminal coronary angioplasty, 2 and 19 +/- 2.4 weeks after percutaneous transluminal coronary angioplasty. Coronary angiography was done in 333 patients (99.7%) (at mean 19 +/- 2.4 weeks). The angiograms were analysed quantitatively., Results: There were no differences in the clinical and angiographic characteristics among the groups except for age. The non-smokers were older than the smokers (55.7 vs 52.4 years (P = 0.001)). Exercise capacity was equal before percutaneous transluminal coronary angioplasty in both groups (17.6 vs 16.5 W x min-1 x kg-1). Non-smokers had a significantly higher increase in exercise capacity than smokers from baseline to 2 weeks after percutaneous transluminal coronary angioplasty (mean difference 4.3 W x min-1 x kg-1 (95% CI: 2.3 to 6.2; P < 0.001)), and from baseline to 19 weeks after percutaneous transluminal coronary angioplasty (mean difference 3.9 W x min-1 x kg-1 (95% CI: 1.6 to 6.2; P < 0.001)., Conclusion: A clinical benefit from percutaneous transluminal coronary angioplasty was seen in both groups as judged from exercise testing. Smokers had a substantially lower increase in exercise capacity than non-smokers, indicating an attenuated benefit from percutaneous transluminal coronary angioplasty among smokers.

Allograft vascular disease is a significant cause of death of cardiac transplant recipients after the first year of transplantation. With few exceptions, angina pectoris does not develop and objective examinations, including coronary angiography, are necessary to diagnose coronary arteriopathy. Between 1983 and 1994, 214 heart transplantations in 211 patients were performed in our unit. All survivors had coronary angiography performed yearly. Thirty patients had significant localized arterial stenoses. Twelve patients with critical stenosis were accepted for percutaneous transluminal coronary angioplasty. Five patients underwent retransplantation due to progressive graft vascular disease with development of congestive heart failure. Conventional revascularization with transluminal coronary angioplasty can safely be performed with primary good results. In selected patients, retransplantation is an option if patients otherwise fulfil standard criteria for cardiac transplantation.

Iodixanol is a new nonionic, dimeric contrast medium. With the addition of 18 mmol/l Na+ and 0.3 mmol/l Ca++ to iodixanol 320 mg I/ml a plasma-isotonic solution was obtained. The purpose was to evaluate the suitability of iodixanol for use in cardioangiography by determining the diagnostic efficacy, patient tolerability, and cardiac and renal side-effects. Initially, 14 patients with coronary artery disease were examined using iodixanol. A double-blind, randomized study was then performed in 72 patients, comparing iodixanol and iohexol. Serum and urine were sampled before the examination, and one and 2 days after. The diagnostic information was good and the number of adverse events low with iodixanol. The patients reported significantly less of a sensation of warmth following injection of iodixanol than iohexol. Our results also indicate that iodixanol 320 mg I/ml influences renal function to a lesser degree than does iohexol 350 mg I/ml. We therefore conclude that isotonic iodixanol is a safe contrast medium for use in cardioangiography.

Restenosis after percutaneous transluminal coronary angioplasty was demonstrated in 61 (29%) of 210 successfully treated patients. Mostly it occurred within 4 months after treatment and in arteries less than 3 mm in diameter. Careful clinical follow-up is therefore particularly important early after angioplasty of smaller arteries. Redilation can be performed without increased risk of restenosis.

Angiography of 169 patients who had been treated successfully with PTCA showed restenosis in 61. Of these, 38 were successfully treated with a new PTCA, and six developed a new restenosis. Restenosis usually appears during the first four months after PTCA in vessels with a diameter less than three millimeters. The authors emphasize the importance of careful clinical follow-up.

The occupational status of a group of 100 male patients, 35 to 68 years of age, with chronic ischaemic heart disease was studied, and related to the severity and distribution of coronary artery stenosis seen on the arteriograms and to left ventricular function. In this series of patients 31 per cent were working, 31 per cent were recorded as temporarily sick, and 38 per cent as permanently disabled. It appears that while the type of previous occupation and physical activity associated with the job were of importance, there was no correlation between employability on the one hand and severity and distribution of coronary artery disease on the other. 'Blue-collar' workers had a higher rate of unemployment than those in 'white collar' occupations, but this could not be explained by differences in severity of coronary artery disease.

Serum HDL2 concentration has been shown to be lowered in patients with coronary heart disease (CHD). Since we previously reported that serum HDL2 can be estimated by single radial diffusion in agar containing an extract of Staphylococcus capitis, it seemed of interest to study whether serum HDL2 as estimated by this method is different in CHD patients and controls. It was shown that relative activity of HDL2, assessed by the method, was appreciably lower in 40 men with angiographically proven coronary artery disease (CAD) than in a control group of 39 men of the same age. Also apolipoprotein A (apo A) concentration was lower in the CAD group, but group difference in HDL2 activity was greater than separation based upon apoA. It is suggested that precipitation with an extract of Staphylococcus capitis might be a useful approach to estimate serum HDL2 levels.

The effect of verapamil (Isoptin) on coronary hemodynamics was studied in 18 patients with coronary heart disease. The continuous infusion thermodilution technique was used to measure cardiac venous blood flow. At rest, verapamil produced a 13% decrease in coronary arteriolar resistance, a 5% decrease in coronary arteriovenous oxygen difference and a 19% increase in left ventricular efficiency index. No significant effect was noted on myocardial blood flow, oxygen consumption or oxygen consumption per unit of left ventricular pressure work. No change occurred in any of the measured parameters during a submaximal stress test after drug administration. The findings are discussed in relation to the general hemodynamic effects of the drug. It is concluded that verapamil is a mild coronary vasodilator and that myocardial oxygen consumption, in relation to performed left ventricular work, is unaltered by the drug up to a near-maximal work-load.

The reproducibility of myocardial ischaemia provoked by atrial pacing was studied in two groups of patients. The heart rate was slowly increased (10 beats per fourth min) until angina in group A, and quickly increased (10 beats per 20 s) in group B. Cardiac venous flow was measured by thermodilution and blood was sampled for metabolic studies at rest and during the maximum obtained heart rate and repeated after 20 min of rest. Ischaemia was defined as a reduction in myocardial lactate extraction ratio by 50% and to a ratio lower than 0.15. Lactate metabolism changed from production (-0.06 +/- 0.05) during the first pacing to extraction (0.05 +/- 0.05) during the second in group A (p less than 0.02). Lactate metabolism was quite reproducible in group B. All the other metabolic and haemodynamic parameters were unchanged in both groups. We conclude that the duration of atrial pacing is important for the reproducibility of pacing-induced myocardial ischaemia.

In a six-year period (1982-1987), 248 patients were treated with 297 procedures (percutaneous transluminal coronary angioplasty, PTCA) on 282 vessels. Two hundred and fifty-nine (87.2%) of the procedures in 210 (76.7%) of the patients appeared successful angiographically. Thirty-eight procedures were unsuccessful due to failure to pass the stenosis in 18 patients, dissection or occlusion of the treated vessel in 11, and significant residual stenosis in 9 patients. Emergency operations were performed after 11 (3.7%) of the procedures. Two patients died postoperatively. Myocardial infarction was seen in 13 patients, of whom 4 developed pathologic Q-waves in their ECG. Restenosis occurred in 60 (28.6%) of the patients. In the last year of the study, the patients selected for PTCA were in a poorer state angiographically, but the results of PTCA were better, without any increase of the complication rate. Our results, which are in accordance with others, support the concept that PTCA is a relatively safe procedure with a primary success rate of almost 90 percent. However, approximately one third of the patients developed restenosis, which in most cases occurred within 3 months.

The immediate haemodynamic and electrophysiologic effects of intravenous prenalterol 2.5-75 micrograms/kg in patients with coronary heart disease without clinical heart failure were investigated during fixed rate atrial pacing. Right ventricular peak dP/dt increased pronounced and serum concentration dependent after prenalterol concomitant with an increase in stroke volume and a moderate decrease in peripheral vascular resistance. The effects on haemodynamics after prenalterol were thus serum concentration dependent but with marked interindividual variation. AV nodal conduction velocity increased significantly. It is concluded that prenalterol possess pronounced inotropic properties. The haemodynamic response to prenalterol intravenously is to a lesser degree dependent on the chronotropic effects of the drug and it is often unpredictable.

The human anterior left ventricular circulation was investigated at rest and during submaximal atrial pacing by measuring the great cardiac venous blood flow by the constant infusion thermodilution method. Forty-seven patients with angina pectoris participated in the study and were grouped stepwise according to degree of arteriosclerosis in the left anterior descending coronary artery (LAD), from normal to occluded vessel. Special attention was paid to patients with earlier infarcts and to collateral circulation. Blood flow to the myocardium was slightly but significantly reduced only among patients with a subtotal stenosis of the LAD without demonstrable collateral circulation, and only during atrial pacing. This conforms with an increased coronary arteriolar resistance in these patients. Myocardial oxygen extraction was, however, increased in all groups of patients with LAD stenosis from 50% to occlusion, except in patients with an earlier anterior wall myocardial infarction. This suggests a disproportion between oxygen demand and blood flow leading to increased extraction in patients without infarcts and a shunting of blood through scarred myocardium with a low oxygen demand in those with a previous necrosis, and is confirmed by a decreased ratio between myocardial flow and cardiac work. Patients with an increased oxygen extraction may benefit from coronary bypass surgery to the LAD area while those without may not.

In 80 male patients with coronary heart disease maximum diastolic pressure in the left ventricle (LVMDP) (usually the top of the a wave), and 'post a' end-diastolic pressure (LVEDP) before and 2 and 3 minutes after ventriculography were correlated to angiographic estimates of left ventricular function (aneurysm, ejection fraction (EF), and to lesions shown by selective coronary arteriography using a score system (coronary artery lesions index, CALI). A significant correlation between CALI and LVEDP (or LVMDP) could not be shown either before or after ventriculography. Before ventriculography, however, LVEDP and LVMDP were good predictors of left ventricular dyskinesia (aneurysm and/or EF less than 50%). A positive and significant correlation between CALI and the LVEDP (and LVMDP) increments following ventriculography (delta LVEDP, delta LVMDP) was found in patients with LVEDP (or LVMDP) below 12 mmHg before ventriculography. Using delta LVEDP the correlation coefficient was 0-51 (n = 41, P less than 0-001, 95 per cent confidence interval 0-24 to 0-88). Using delta LVMDP r = 0-47 (n = 41, 0-001 less than P less than 0-01). Delta LVEDP greater than 12 mmHg was found only in patients with triple vessel disease.

Effects of the new Ca++ antagonist nifedipine (Adalat) on coronary haemodynamics were studied in 8 patients with documented ischaemic heart disease. The continuous infusion thermodilution technique was used to measure cardiac venous blood flow. Sublingual application of 10 mg nifedipine caused a significant increase (16%) in myocardial blood flow and a decrease (18%) in coronary arteriolar resistance at rest, but not during a submaximal atrial pacing test. There was no change in coronary arteriovenous oxygen difference, myocardial oxygen consumption, oxygen consumption per unit of heart rate blood pressure index or left ventricular efficiency index. The effects on the coronary haemodynamics are discussed in relation to the simultaneous changes in general haemodynamics. Systolic aortic pressure was slightly reduced, significantly only at rest, while peripheral vascular resistance decreased and cardiac output increased also during atrial pacing. No change in free fatty acid metabolism was observed. It is concluded that nifedipine is a mild coronary vasodilator. No effect was observed on myocardial oxygen demand. The oxygen cost of left ventricular work was unchanged by the drug both at rest and during the submaximal stress test.

Myocardial metabolism was studied during coronary vasodilatation by carbocromen during atrial pacing in patients with coronary arteriosclerotic disease. Coronary sinus flow was measured by the continuous infusion thermodilution technique. Carbocromen increased myocardial flow by the same amount at rest and during pacing-induced tachycardia. The administration of carbocromen did not interfere with myocardial oxygen consumption, free fatty acid (FFA) uptake, pulmonary or systemic hemodynamics. Atrial pacing above the anginal threshold increased lactate and hypoxanthine excretion to the coronary sinus, but to a greater extent during carbocromen treatment. Thus, carbocromen is a specific coronary vasodilator acting independently of pacing induced vasodilatation. Metabolic data indicate a small but unfavourable effect on ischemic metabolism which might be due to a "coronary steal".

Monophasic action potentials were recorded in the outflow tract of the right ventricle in patients with coronary artery disease during ventricular pacing at different basic cycle lengths and programmed stimulation. During continuous pacing (basic cycle length 600 ms) the time for 90% repolarisation (MAP90) and the QTa interval decreased exponentially during the first 1.5-2 min of pacing to 90% of control values. The reproducibility of the monophasic action potential signals and the ventricular effective refractory period were assessed as good when studied after repetitive trains of 8 beats for more than 1.5 min. The reproducibility of conduction, however, was less good. Electrical restitution of MAP90 duration of the premature beats determined at three different basic cycle lengths was different from that in single muscle preparations. The curves showed two phases with unchanged MAP90 durations despite longer coupling intervals. The first phase was close to the ventricular effective refractory period, probably because subnormal conduction left the diastolic interval constant for the earliest premature beats. This indicates that subnormal conduction may influence the premature dispersion of repolarisation.

Duplex scanning of the lower thoracic aorta was performed on 67 patients subjected to routine left and right heart catheterization with estimation of cardiac output ad modum Fick. Adequate Doppler signals from the lower thoracic aorta were obtained in 59 patients (88%), 26 of whom had aortic valve abnormality. A high correlation was found between the Doppler and Fick findings (r=0.89), with a regression line intercepting close to zero (cardiac output = 1.76 X Doppler flow +0.05). The presence of aortic valve abnormality did not seem to influence the accuracy of the Doppler flow results. It is concluded that Doppler flowmetry in the lower thoracic aorta is a useful method in estimation of resting cardiac output, especially in patients with aortic valve lesions making Doppler flowmetry in the ascending aorta impossible.

In a double-blind, randomized, two-group study of 99 'high-risk' patients mainly with coronary artery disease, the non-ionic contrast medium, Amipaque (metrizamide), was compared with the ionic medium, Isopaque Coronar (meglumine-Na-Ca-metrizoate) in cinecardioangiography. In evaluating the influence of the contrast media on the left ventricular end diastolic pressure (LVEDP), the material was divided into 2 groups, 55 patients with a basal LVEDP of 15 mmHg or less and 44 with an LVEDP above this level. In the former group LVEDP increased significantly after injection of the contrast medium into the left ventricle, but significantly less (p = 0.006) after Amipaque than after Isopaque Coronar. In the patients with a basal LVEDP above 15 mmHg, no significant change occurred in LVEDP after left ventriculography with any of the 2 contrast media. No serious complications occurred.