PubMed Health⌕ Search

Biomedical subjects

J P Bagger

Publications and source records attributed to J P Bagger.

At least 91 records · Page 5Linked to original sources

Atrial natriuretic peptide during pacing in controls and patients with coronary arterial disease.

At rest, during cardiac catheterization, aortic plasma levels of immunoreactive atrial natriuretic peptide did not differ between 10 controls with atypical chest pains and normal coronary arteries and 9 patients with stable angina pectoris and coronary arterial disease (55.2 +/- 19.8 vs. 64.8 +/- 19.8 pg/ml, NS). Nor did atrial natriuretic peptide values differ between the two groups during or after atrial pacing (150 beats/minute), which induced electrocardiographic and metabolic signs of acute myocardial ischaemia in the patients with coronary arterial disease but in none of the controls. Pacing, when carried out for more than 300 seconds, induced an increase of plasma atrial natriuretic peptide that correlated with duration of pacing (r = 0.80, P less than 0.001), and similarly in controls and patients with coronary arterial disease. In a second part of the study, which included 2 controls and 2 patients with coronary arterial disease, post-pacing coronary sinus concentrations of atrial natriuretic peptide were 10-20 times higher than peripheral levels (415- greater than 890 pg/ml). The concentration of atrial natriuretic peptide rose as blood from the caval veins (34 +/- 7 pg/ml) entered the right atrium (56 +/- 24 pg/ml), but thereafter was unchanged in the pulmonary artery (51 +/- 3 pg/ml) and the aorta (46 +/- 9 pg/ml). In conclusion, the results gave no evidence for ischaemic heart disease without congestive cardiac failure to be associated with altered levels of atrial natriuretic peptide. It was confirmed that atrial pacing stimulates the secretion of atrial natriuretic peptide which is produced by the heart and released via the coronary sinus into the circulation.

Atrial Natriuretic Factor↗

Dose-related haemodynamic effects of nicardipine during rest and exercise and variable anti-anginal effects in patients with chronic stable angina.

The effects of increasing doses of i.v. nicardipine (2.5, 5.0 and 7.5 or 10.0 mg) on blood pressure, heart rate and exercise performance were studied in 12 patients with chronic effort angina. Plasma nicardipine concentrations correlated closely with the infused doses (r = 0.90). Resting haemodynamic changes after nicardipine included a dose-related fall in systolic (5%, 13%, 15%) and diastolic (0%, 6%, 8%) blood pressure and a rise in heart rate (10%, 19%, 30%). Rate-pressure product was slightly increased after the highest dose (10%). During exercise, maximal systolic blood pressure decreased (3%, 9%, 9%) and heart rate increased (2%, 4%, 9%) but the rate-pressure product remained unchanged. Exercise tolerance improved in 10 patients as indicated by prolonged exercise duration in all, delayed appearance of ST-segment depression in 6, decreased maximal ST-segment depression in 5, and abolished (N = 3) or diminished (N = 4) anginal pain at the end of exercise after optimal nicardipine dose. Five of the 10 patients obtained maximum benefit after the highest dose. The other five patients improved after 2.5 or 5.0 mg but deteriorated (N = 4) or had no further benefit when the dose was increased (N = 1). One patient deteriorated even after the lowest dose, whereas one patient neither improved nor deteriorated after any dose. The patients who deteriorated after low or high doses tended to be more severely diseased than those who tolerated the maximal dose well. The results stress the importance of individual dose titration of nicardipine to ensure maximum benefit in patients with chronic effort angina.

Angina Pectoris↗

Vasospastic angina assessed by hyperventilation-thallium-201 myocardial scintigraphy.

The response to prolonged hyperventilation (HVT) was evaluated by electrocardiography (HVT-ECG) and thallium-201 myocardial scintigraphy (HVT-Tl-Sc) in 40 patients suspected of vasospastic angina. Both tests showed ischaemic changes in 16 patients and no changes in 20 patients. Two patients had abnormal HVT-ECG and normal HVT-Tl-Sc, and the reverse combination was found in two patients. Prolonged HVT was performed in 14 patients during coronary angiography (CAG). Nine developed transient total or subtotal occlusion in one of the major coronary arteries, all of whom had ischaemic HVT-ECG and eight had abnormal HVT-Tl-Sc. In the five patients without spasm at CAG four had normal HVT-ECG and all five normal HVT-Tl-Sc. Our data suggest that HVT-ECG and HVT-Tl-Sc have essentially the same sensitivity and specificity in detecting vasospastic angina.

Adult↗

Electrical injury causing ventricular arrhythmias.

Dangerous or long lasting ventricular arrhythmias developed in three patients who had sustained an electrical injury in which current passed through the thorax. In all three cases there was a delay of 8-12 hours between the injury and the onset of symptoms. The ventricular arrhythmias were severe and long lasting. In two of the three patients, ventricular tachycardia or ventricular fibrillation or both occurred and in one patient ventricular parasystole developed. No enzymatic evidence of myocardial necrosis was found but the results of an endomyocardial biopsy carried out in two of the three patients showed focal myocardial fibrosis and increased numbers of Na, K-pumps. The two patients with ventricular tachycardia became symptom free after appropriate antiarrhythmic treatment and in the third patient ventricular parasystole disappeared spontaneously within two years. Patients sustaining electrical injury in which current passes through the thorax should be monitored electrocardiographically for at least 24 hours, and patients with unexpected arrhythmias should be questioned about previous electrical injury.

Adult↗

Myocardial substrate utilization and amino acid metabolism in chronic coronary artery disease.

Patients with typical effort angina have been considered to have normal myocardial metabolism at bodily rest (24). In contrast to this, the present study demonstrated, even in resting asymptomatic CAD patients, a decreased myocardial uptake of FFA, independent of arterial levels and probably reflecting a decreased capacity for FFA oxygenation. This was compensated for by increased aerobic, and in some cases anaerobic, carbohydrate utilization. Further more, there was increased alanine release and glutamate uptake, related to, and perhaps of importance for the maintenance of increased carbohydrate breakdown. The altered myocardial substrate preference related to the severity of ischemic disease, indicates a metabolic adaptation induced by chronic myocardial ischemia in CAD patients.

Amino Acids↗

Whole blood versus plasma measurements of glutamate and alanine across the human myocardium.

Comparison of whole blood and plasma aorto-coronary sinus concentration differences of glutamate and alanine were made before, during and after coronary sinus pacing in seven patients with normal and six patients with stenotic coronary arteries. Mean differences between duplicate analyses were greater in whole blood than plasma both of glutamate (7.5 +/- 5.8 vs. 3.3 +/- 3.0 mumol/l, p less than 0.001) and of alanine (7.9 +/- 7.0 vs. 3.8 +/- 3.4 mumol/l, p less than 0.001). Concentrations of glutamate were 3.4 and of alanine 1.4 times higher in whole blood than in plasma. Blood cells were calculated to be responsible for about 20% of glutamate and alanine blood exchanges across the heart. Plasma and whole blood fluxes were closely positively correlated (glutamate:r = 0.81, alanine:r = 0.88) and had always the same direction. Differences in myocardial exchanges of amino acids between the patients with and without coronary artery disease, as well as rapid changes during pacing, could be demonstrated in plasma analyses but were not significantly reflected in whole blood glutamate determinations. This seemed to be due to the greater variations in whole blood analysis. In conclusion, differences in aorto-coronary sinus plasma concentrations reflected, although underestimated, whole blood fluxes. Because of considerable gains in precision of analysis, plasma should be preferred to whole blood for evaluations of glutamate and alanine exchanges across the human heart.

Adult↗

Oesophageal spasm in patients with coronary artery spasm.

Oesophageal manometry was performed in 20 patients with chest pain, of whom 10 showed coronary artery spasm (group I) and 10 did not (group II). In the basal state oesophageal spasms were recorded in 6 patients from group I but in none from group II (p less than 0.05). In group I the duration of oesophageal contractions was 4.50 +/- 0.65 s compared with 2.86 +/- 0.36 s in group II (p less than 0.05). Prolonged hyperventilation was performed during manometry by 7 patients from each group. In group I this caused chest pain in all 7, with electrocardiographic changes in 6; at the same time oesophageal spasms were intensified in 5 patients and began anew in 1. In group II no electrocardiographic changes were seen with hyperventilation, and 1 patient showed oesophageal spasm. These observations suggest a relation between spasm of the coronary arteries and spasm of the oesophagus.

Adult↗

Angiotensin-converting enzyme and coronary haemodynamics in coronary artery disease.

Coronary sinus pacing was performed in 12 patients with and 12 patients without significant coronary artery disease as verified by angiography in order to elucidate a possible link between cardiac exchange of angiotensin-converting enzyme and the coronary circulation. The coronary sinus and arterial blood enzyme activity remained unchanged and were similar in the two groups, both at rest and during pacing, and the activity was not related to pacing-induced changes in oxygen consumption or coronary vascular resistance. Therefore it does not seem that global cardiac formation or depletion of angiotensin-converting enzyme is of regulatory importance in the coronary vascular bed in patients with and without coronary artery disease under these circumstances.

Adult↗

Exercise stress testing in angina patients with positive response to hyperventilation testing: influence of the coronary artery tone.

We studied the exercise stress test and the coronary artery tone in two groups of angina patients with comparable coronary atherosclerosis. Group I (20 males and 5 females, mean age 53.5 years) with a positive, and group II (22 males and 3 females, mean age 52.5 years) with a negative response to the hyperventilation test (HVT). A positive exercise stress test (ST depression greater than or equal to 1 mm) was found in 24 patients in group I vs. 15 in group II (p less than 0.01), despite a lower maximal rate pressure product (198 +/- 11.2 vs. 236 +/- 10.1, p less than 0.05) and maximal work load (110 W +/- 7.1 vs. 136 +/- 7.4 W, p less than 0.02) in group I. A high coronary artery tone (dilatation (DIL%) of the coronary arteries after nitroglycerin greater than or equal to 10%) was found in 18 patients in group I and in 4 in group II (p less than 0.01). DIL% was 22.6 +/- 3.8 vs. 5.8 +/- 1.4 in groups I and II, respectively (p less than 0.005). DIL% was significantly related to persistence of ST depression after exercise (r = 0.36, p less than 0.05), and 21 of 22 patients with high tone had a positive exercise stress test vs. 18 of 28 with low tone (p less than 0.05). These findings suggest that the coronary artery tone influences the response to exercise in some patients with angina. Since the patients in group I were identified by HVT, our results underline the clinical relevance of this test.

Angina Pectoris↗

Improved myocardial lactate extraction after propranolol in coronary artery disease: effected by peripheral glutamate and free fatty acid metabolism.

Ten patients with chronic effort angina and coronary artery disease (luminal diameter reduction greater than 75%) were stressed by atrial pacing (140 beats/minutes) before and 15 minutes after intravenous propranolol (mean dose 7.4 mg). Myocardial substrate exchange of oxygen, blood lactate, plasma free fatty acids, citrate, glucose, glutamate, and alanine as well as coronary sinus blood flow were measured. Coronary sinus blood flow, oxygen consumption, and systemic haemodynamics did not change after propranolol. Propranolol did not influence arterial lactate concentration, and it reduced the arterial concentration of free fatty acid by 37% and increased that of glutamate by 21%. During pacing myocardial lactate extraction increased in all 10 patients; in two lactate release was converted to lactate uptake. Propranolol reduced free fatty acid uptake and increased glutamate uptake during pacing. For both substances the changes in aortocoronary sinus differences or in uptake or both correlated positively with the changes in their delivery to the heart from extracardial sources (arterial concentrations/loads). In the unstressed state before pacing, aortocoronary sinus lactate differences correlated inversely with free fatty acid differences and positively with those of glutamate. During pacing the relation between lactate and glutamate differences remained positive while the inverse correlation between lactate and free fatty acid differences was lost. Myocardial citrate release was halved during pacing and recovery. Propranolol did not influence alanine or glucose exchanges. An improved myocardial lactate extraction after propranolol administration may be secondary to decreased free fatty acid uptake or increased glutamate uptake or both. In the unstressed state both mechanisms may be of importance. During pacing induced ischaemia, increased glutamate uptake is more likely than reduced free fatty acid uptake to be the mechanism responsible for the improvement in myocardial lactate extraction. The propranolol mediated alterations in myocardial substrate exchanges may reflect the extracardial effects of the drug.

Adult↗

Transdermal nitroglycerin (Transiderm-Nitro) in the treatment of unstable angina pectoris.

Eighteen patients, 13 male and five female, with unstable angina pectoris and who had greater than or equal to 3 anginal attacks/day despite treatment with beta- and/or Ca-blockers were treated for three days with transdermal nitroglycerin (Transiderm-Nitro 25 mg/24 hours) in a randomised, placebo-controlled trial. A significant reduction of anginal attacks (p = 0.03) was demonstrated only during the first day of treatment. The lack of significant effects during the following two days was ascribed partly to the possible development of nitrate-tolerance, partly to a declining number of anginal attacks in the placebo-group during the trial period, for which reason the difference between the actively treated and the placebo group became smaller and finally the consumption of nicomorphine was considerably greater in the placebo group.

Administration, Cutaneous↗

Transseptal left heart catheterization with a Swan-Ganz flow-directed catheter: review of 173 studies.

Of 178 transseptal left heart catheterizations performed, 173 successful cases are reported, with the use of a Swan-Ganz, flow-directed, balloon-tipped catheter. By means of a modified Brockenbrough technique, which is described in detail, a 10F Teflon tube (3.3 mm outside diameter) was inserted into the left atrium. Through the tube, which was continuously flushed with saline solution, a 5F Swan-Ganz catheter was introduced into the left atrium. In all cases where left atrial puncture was possible (n = 173), the left ventricle was easily entered, even in the presence of mitral stenosis. Two major complications with signs of cerebral embolism occurred in this series. The method is technically reliable and acceptably safe in cases where the transseptal route of left heart catheterization is required.

Adolescent↗

Coronary sinus blood flow determination by the thermodilution technique: influence of catheter position and respiration.

By measuring the coronary sinus blood flow using the thermodilution technique the influence of "thermodilution catheter" withdrawal from the great cardiac vein to the ostium of the coronary sinus was investigated in 41 patients. In addition, the influence of normal and forced respiration on coronary sinus blood flow was measured in 16 of the patients. Mean great cardiac vein flow was measured to 54 +/- 25 ml X min-1. Catheter withdrawal revealed coronary sinus blood flows of 80 +/- 32, 103 +/- 35, 145 +/- 39 and 213 +/- 61 ml X min-1 when the catheter was moved by steps of 1 cm towards the coronary sinus ostium. The coronary sinus blood flow changed between 116 +/- 34 ml X min-1 and 128 +/- 41 ml X min-1 on expiration or inspiration during normal respiration, respectively, when the catheter was placed in a mid-coronary sinus position. Forced respiration changed the coronary sinus blood flow from 98 +/- 41 ml X min-1 during expiration to 196 +/- 76 ml X min-1 during inspiration. The data show that coronary sinus blood flow changes from 23 to 68 ml X min-1 per cm catheter movement, the nearer the ostium the greater the change. Therefore comparison of coronary sinus blood flow between groups of patients would be a comparison between different catheter positions. Normal respiration moves, as judged by the coronary sinus blood flow, the thermodilution catheter by less than 0.5 cm while forced respiration moves the catheter up to 2 cm within the coronary sinus.

Adult↗

Verapamil induced increment of oxygen extraction in the arteriosclerotic limb.

The acute effect of intravenously administered verapamil (0.08 mg X kg-1 body weight, mean dose 5.1 +/- 0.7 mg) on oxygen exchange and arterial blood flow (measured electromagnetically) of the lower limb was studied during reconstructive arterial surgery in 17 patients with obliterative arterial disease of the lower limbs. Verapamil increased oxygen extraction in the diseased leg by 12% (from a median value of 28.3 to 31.6 ml X litre-1, p less than 0.01) whereas it had no effect on arterial blood flow. The increment of oxygen extraction after drug administration correlated negatively with the walking distance of the patients (r = 0.69, p less than 0.01). Systolic and diastolic blood pressure decreased significantly by 10% and 6%, respectively, whereas heart rate remained unchanged after the administration of verapamil. The results suggest that verapamil might be beneficial in the treatment of patients with intermittent claudication, despite the fact that no vasodilatation was seen after the drug.

Aged↗

Influence of nifedipine on coronary haemodynamics and myocardial metabolism in coronary artery disease.

The effect of 30 mg sublingual nifedipine on cardiac metabolism and haemodynamics was studied during two identical periods of pacing in 11 patients with chronic coronary artery disease. The pace time to angina pectoris improved after nifedipine in 6 patients, deteriorated in 2 and was unchanged in 3. Nifedipine decreased blood pressure (12%), rate pressure product (10%) and coronary vascular resistance (17%) during pacing. Aorto-coronary sinus (A-Cs) oxygen difference decreased at rest (9%) and postpacing (10%) after nifedipine, although an opposite tendency in coronary sinus blood flow resulted in unchanged myocardial oxygen uptake throughout the study. Although mean myocardial lactate extraction after nifedipine was unchanged during pacing in the whole group of patients, it increased in 9 patients who showed a net lactate release at control pacing (from -50.9 +/- 33.5% to -35.9 +/- 30.2%, P less than 0.05). Nifedipine increased free fatty acid (FFA) extraction during pacing (from 1.5 +/- 12.9% to 17.4 +/- 13.1%, P less than 0.02) and uptake (from 1.8 +/- 8.5 to 11.1 +/- 10.6 mu mol min-1, P less than 0.05). Nifedipine influenced only glucose exchange significantly (46% decreased extraction) at 5 min postpacing. The A-Cs citrate gradient lessened 30-40% postpacing after nifedipine administration. Since the unloading effects of nifedipine did not alter myocardial oxygen uptake, the most important net haemodynamic finding was the decrease in coronary vascular resistance. Although no significant antianginal effect of a fixed dose of nifedipine was found, the increased uptake of FFA may reflect improved myocardial oxidative metabolism after nifedipine.

Angina Pectoris↗

Vasospastic ischaemia induced by the hyperventilation test in patients with a negative response to ergometrine.

We present the case histories of two patients with angina pectoris who developed coronary artery spasm in response to provocation with prolonged hyperventilation (verified by ST segment elevation in both and coronary angiography in one) despite a negative ECG response to intravenous injection of 0.4 mg ergometrine. This new observation, which is in conflict with recent publications stating that ergot provocation is more sensitive than hyperventilation, suggests that in some patients diagnostic provocation with hyperventilation may be an alternative to the widely used ergot provocation.

Adult↗