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Background: Perinatal asphyxia is associated with cardiac dysfunction secondary to myocardial ischaemia. Cardiac troponin I (cTnI) is a marker of myocardial necrosis. Raised concentrations in the blood are related to perinatal asphyxia and increased morbidity.Objective: To assess porcine myocardial damage from enzyme release during hypoxaemia induced global ischaemia, and subsequent resuscitation with ambient air or 100% O(2). To investigate whether CO(2) level during resuscitation influences myocardial damage.Design: Newborn piglets (12-36 hours) were exposed to hypoxaemia by ventilation with 8% O(2) in nitrogen. When mean arterial blood pressure had fallen to 15 mm Hg, or base excess to < -20 mmol/l, the animals were randomly resuscitated by ventilation with either 21% O(2) (group A, n = 29) or 100% O(2) (group B, n = 29) for 30 minutes. Afterwards they were observed in ambient air for another 150 minutes. During resuscitation, the two groups were further divided into three subgroups with different CO(2) levels.Analysis: Blood samples were analysed for cTnI, myoglobin, and creatine kinase-myocardial band (CK-MB) at baseline and at the end of the study.Results: cTnI increased more than 10-fold (p < 0.001) in all the groups. Myoglobin and CK-MB doubled in concentration.Conclusion: The considerable increase in cTnI indicates seriously affected myocardium. Reoxygenation with 100% oxygen offered no biochemical benefit over ambient air. CK-MB and myoglobin were not reliable markers of myocardial damage. Normoventilation tended to produce better myocardial outcome than hyperventilation or hypoventilation. [ABSTRACT FROM AUTHOR]

Unlabelled: The main purpose of this study was to investigate whether circulating natriuretic peptides in premature infants reflect the hemodynamic significance of a patent ductus arteriosus (PDA). The study comprises 120 examinations in 55 premature infants with a mean gestational age of 27.2 wk and a mean birthweight of 933 g. Based on clinical and echocardiographic findings, the hemodynamic influence of ductal shunting was classified as small, moderate or large. Blood samples for N-terminal proatrial natriuretic peptide (Nt-proANP) and brain natriuretic peptide (BNP) were analysed after completion of the clinical part of the study. Linear regression indicated a very strong association between Nt-proANP and BNP (adjusted R = 0.89). The mean levels of Nt-proANP and BNP increased with the size of the shunt through a PDA, and peptide values followed hemodynamic alterations. The size of PDA accounted for 50% and 47% of the total variation in the plasma values of Nt-proANP and BNP, respectively. In detecting an echocardiographically significant PDA, the area under a ROC curve was 0.94 for Nt-proANP and 0.90 for BNP.Conclusion: The magnitude of shunting through a PDA is the main determinant of plasma levels of natriuretic peptides in premature infants. Nt-proANP and BNP seem to have the same pattern of secretion. Our findings indicate that measurements of natriuretic peptides may provide clinically relevant information in the hemodynamic assessment of premature infants. [ABSTRACT FROM AUTHOR]

Objectives: A marked, sequential decline in coronary heart disease (CHD) mortality is established, but not its causes. Does it reflect modern treatment effects or a spinoff of primary prevention? The aim of this study was to explore this issue using a prospective cohort follow-up design.Design: In 1972-1975 and 1980-1982 Cohorts 1 (n = 613) and 2 (n = 667) of identical age (males, mean 56 years) were examined, and thereafter followed closely for 14 years. CHD risk- and treatment patterns, incidence of non-fatal myocardial infarctions (MIs) and total-, cardiovascular and CHD mortality rates were studied.Results: CHD risk factors were more favourable, medical treatment more aggressive and 14-years CHD mortality, as expected, lower in Cohort 2 (7.7%/4.8%, p = 0.032). However, hospital- and prospective ECG data revealed opposite trends in non-fatal cohort CHD incidence, and aggregated numbers of CHD deaths and non-fatal MI cases were 16.7%/16.0% in Cohort 1/2 (p = 0.90).Conclusions: A marked, sequential reduction in CHD mortality was followed by a reciprocal increase in non-fatal MIs. This phenomenon may prevail in low CHD-endemic areas, and may call for altered primary preventive measures for reduction in total CHD incidence. [ABSTRACT FROM AUTHOR]

Aims Since atherosclerosis is a chronic inflammation and the erythrocyte sedimentation rate is an appropriate test for monitoring chronic inflammatory responses, we wanted to investigate whether the erythrocyte sedimentation rate might carry prognostic information on the risk of sustaining coronary heart disease events.Method The erythrocyte sedimentation rate was determined in 2014 apparently healthy men aged 40–60 years during an extensive cardiovascular survey in 1972–75, and the test was repeated in an identical follow-up examination 7 years later. Cause-specific mortality and rates of non-fatal myocardial infarction were followed for 23 years.Results The erythrocyte sedimentation rate was strongly correlated with age, haemoglobin level, smoking status, total cholesterol level and systolic blood pressure. After adjusting for all these associations in multivariate Cox regression analyses, the erythrocyte sedimentation rate emerged as a strong short- and long-term predictor of coronary heart disease mortality, particularly in men who had developed angina pectoris and/or had a positive exercise ECG test at the second survey. Increases in non-coronary heart disease deaths and in non-fatal myocardial infarctions were only seen in the upper erythrocyte sedimentation rate range.Conclusions The erythrocyte sedimentation rate is a strong predictor of coronary heart disease mortality, and appears to be a marker of aggressive forms of coronary heart disease. The erythrocyte sedimentation rate probably gives substantial information in addition to that given by fibrinogen on the risk of coronary heart disease death. [ABSTRACT FROM PUBLISHER]

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. [ABSTRACT FROM PUBLISHER]

The peak oxygen uptake ( V˙O2peak) of 196 healthy children and adolescents aged 8–16 years, and 187 children and adolescents (in the same age range) with congenital heart disease (CHD), was measured using a graded treadmill test (Oslo-protocol). The healthy population was tested to assess the reference values that were to be used in the interpretation of the results obtained from patients with CHD. The results revealed that patients with CHD exhibited lower V˙O2peak values, with declining values for boys after the age of 12–13 years. When separated into different diagnostic groups, on average, patients with a chronic pressure overload of the left ventricle and patients with tetralogy of Fallot have lower V˙O2peak values, but make approximately the same progress with age as healthy subjects. Patients with transposition of the great arteries, however, displayed a marked decline in V˙O2peak after the age of 12–13 years. Whether exercise testing should be included in routine follow-up in patients with CHD, especially those between the ages of 10 and 16 years, when the condition of some patients detoriates, requires special attention. [ABSTRACT FROM AUTHOR]

Fifty-eight children and adolescents of both sexes, aged 8-16, were tested on a treadmill using two different protocols. The well-known Bruce-protocol has the disadvantages of steep incline and large increments at each step. A new protocol (Oslo-protocol) with less incline and smaller increments was compared to the Bruce-protocol. The results from the two protocols showed no differences with regard to peak oxygen uptake (VO[sub2peak]) or peak heart rate (HR[subpeak]). However, the respiratory exchange ratio (R) and blood lactate concentration [La[sup-] showed higher values when the Bruce-protocol was used. The study also indicated that the often used criteria of HR[subpeak], R and achievement of a plateau in VO[sub2] to estimate VO[sub2peak], were not reliable indicators in either protocol. When time to exhaustion was used as an estimation of aerobic edurance level, the Oslo-protocol discriminated better than the Bruce-protocol. As a conclusion, the results indicate that none of the criteria may be used as a reliable indicator of having achieved VO[sub2peak]. An experienced test-leader may be essential to define when VO[sub2peak] has been reached in children. On the basis of the results from the current study, the Oslo-protocol seems suitable as a test-protocol when testing children and adolescents for VO[sub2peak]. [ABSTRACT FROM AUTHOR]

AimsTo study the impact of smoking on the change in exercise capacity in patients treated with coronary angioplasty.MethodsThree 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 trans-luminal 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.ResultsThere 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 16·5W×min−1×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 4·3W×min−1×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 3·9W×min−1×kg−1(95%CI: 1·6 to 6·2;P<0·001)).ConclusionA 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. [ABSTRACT FROM PUBLISHER]

Myocardial scintigraphy with thallium-201 and electrocardiogram-gated left ventriculography with technetium-99m labelled red blood cells were applied in four groups of subjects: 25 with no signs or symptoms of cardiovascular disease (group 1), 28 with a "false" positive exercise electrocardiogram (group 2), 14 with angina pectoris and normal coronary angiograms (group 3), and 43 with angina pectoris and fixed coronary artery stenoses (group 4). In groups 1 and 4 the radionuclide findings were in accordance with clinical and invasive measurements. In groups 2 and 3 the most important finding was the lack of increase in left ventricular ejection fraction during exercise in about half of these subjects (even a decrease in 25%), indicating subnormal myocardial reserve. The additional finding of pathological myocardial biopsies in four of these patients suggests that asymptomatic ST depression in patients with normal coronary angiograms may in some cases represent an early, preclinical sign of cardiomyopathy. [ABSTRACT FROM PUBLISHER]

The haemodynamic effects of nifedipine, propranolol, and the combined administration of the two drugs were studied in 12 patients with hypertrophic obstructive cardiomyopathy. The combined administration of nifedipine and propranolol appeared to be superior to that of nifedipine alone. The spontaneous heart rate was reduced in most cases after nifedipine plus propranolol, and at atrial pacing the following results were obtained: left ventricular peak systolic pressure was reduced from 200 +/- 39 to 157 +/- 30 mmHg; a positive correlation was found between the pre-drug left ventricular end-diastolic pressure and the magnitude of reduction in left ventricular end-diastolic pressure; systolic blood pressure was reduced from 125 +/- 31 to 111 +/- 27 mmHg, and total peripheral resistance was reduced from 1403 +/- 307 to 1160 +/- 209 dyne s-1 cm-5. The combined administration reduced the resting left ventricular outflow gradient from 76 +/- 19 to 45 +/- 26 mmHg, while cardiac index was left unchanged. The effects on mean pulmonary arteriolar resistance and mean pulmonary arteriolar resistance and mean pulmonary capillary venous pressure were in most cases slight and insignificant. The results indicate an improved haemodynamic condition in patients with hypertrophic obstructive cardiomyopathy after the combined administration of nifedipine and propranolol: a treatment that might provide a new and useful alternative to already existing medication. [ABSTRACT FROM PUBLISHER]

Sixty-six consecutive patients less than 40 years of age with angiographically documented coronary artery disease and coronary heart disease took part in a study aimed at (1) identifying the presence of factors which might explain the premature onset of ischaemic heart disease, and (2) assessing the distribution and severity of the coronary artery lesions. For comparisons we have used a study of risk factors in 1832 men defined as "normals" according to a recent comprehensive examination. The findings show that the typical early onset coronary heart disease case is an overweight, heavily smoking male "blue collar" worker, with high serum levels, a marginally raised blood pressure, and a high prevalence of coronary heart disease among first degree relatives. Coronary angiography showed a preponderance of one vessel disease. In particular, left anterior descending artery lesions were common, which might have contributed to the early manifestation of disease. [ABSTRACT FROM PUBLISHER]

1 The time-related, comparative beta-adrenoceptor blocking effect of metoprolol 150 mg twice daily, atenolol 100 mg once daily and pindolol 7.5 mg twice daily on heart rate, blood pressure, work performance, blood lactate, free fatty acids and plasma catecholamines was studied in ten males aged 19-25 years by means of repeated maximal bicycle exercise tests. 2 At steady state several differences in effects were noted among the drugs. These could be explained by differences in beta 1-selectivity, potency of the chosen drug-doses and intrinsic sympathomimetic activity (ISA). 3 This study emphasizes the importance of including strong sympathetic stimuli in any model used for comparing beta-adrenoceptor blockers with and without ISA in order not to underrate the effects of beta-adrenoceptor blockers with ISA. 4 In the chosen doses pindolol was more effective, and atenolol less effective than metoprolol in suppressing heart rate and blood pressure responses to maximal exercise. [ABSTRACT FROM AUTHOR]

A positive exercise ECG test in a middle-aged man without confounding disease is a strong indicator of occult coronary heart disease. In the years following a positive lest mortality increases moderately, but CHD events vary considerably compared with subjects having normal exercise tests. If a second exercise test is positive in the same subjects years later, this signifies a disease which is prone to progress in a very severe way in the ensuing years. A first normal test followed by a second pathologic test has an intermediate prognostic significance compared with two normal tests years apart. The clinical course indicates that preventive measures should be taken after observing a positive exercise test, and even more importantly if two positive tests are observed years apart. [ABSTRACT FROM PUBLISHER]

Abstract Background This pilot study (ClinicalTrials.gov ID: NCT01507701) assessed the feasibility and safety of clonidine in adolescent chronic fatigue syndrome (CFS). Specifically, we assessed clonidine dosage in relation to a) plasma concentration levels, b) orthostatic cardiovascular responses, and c) possible adverse effects. Findings Five adolescent CFS patients (14–19 years old) received 50 μg clonidine twice per day during 14 days in an open, uncontrolled design. Plasma concentration of clonidine was assayed by standard laboratory methods. Changes in orthostatic cardiovascular responses were assessed by a 20o head-up tilt-test (HUT). Adverse effects were mapped by a questionnaire. After 14 days, C0 median (range) of clonidine was 0.21 (0.18-0.36) μg/L, and Cmax median (range) of clonidine was 0.41 (0.38-0.56) μg/L. Also, supine blood pressures and heart rate were lower during clonidine treatment, and the HUT response was closer to the normal response. No serious adverse effects were registered. Conclusion Clonidine 50 μg BID seems to be safe enough to proceed from a pilot study to a controlled trial in a select group of adolescents with CFS (ClinicalTrials.gov ID: NCT01040429).