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Biomedical subjects

C Droste

Publications and source records attributed to C Droste.

32 records · Page 2Linked to original sources
PubMed1990

Influence of opiate systems in pain transmission during angina pectoris.

The situation of absent pain with silent myocardial ischemia is highly difficult to define. There are probably several reasons for the lack of pain. Partly, nerve ways may be destroyed, partly, myocardial ischemia as peripheral pain stimulus may be to weak and beyond threshold, however, additionally, there are a lot of clues for the participation of endogenous pain modification systems therein. A certain amount of myocardial ischemia is a necessary, but not sufficient precondition for anginal pain. Myocardial ischemia is only felt painfully if the peripheral nociceptive impulse rate is high enough to pass the actual inhibitory pain threshold, and if the nerve ways are intact. It is generally accepted that the endogenous opiate system, to some extent, takes part in the endogenous analgesia system. A range of examinations in recent years hinted at the fact that endorphins are in relation to the absence of pain in silent ischemia. Patients with symptomatic and asymptomatic myocardial ischemia are significantly different in plasma beta-endorphin levels at rest and during physical exercise. A relation between peripheral endogenous opiates and suffering behavior can, at present, only be indicated correlatively. It is likely that the intensive overlaying of the cardiovascular and pain regulating systems is related to the absence of pain in silent myocardial ischemia.

Adrenocorticotropic Hormone↗
PubMed1989

Silent myocardial ischemia.

Myocardial ischemia can manifest itself as strictly silent or a combination of symptomatic and silent episodes. We have demonstrated that most asymptomatic patients have a higher threshold for pain than did symptomatic patients. Low sensitivity to pain in patients with silent ischemia may be related to both a neural pain inhibitory system and the release of endogenous opiates, the endorphins. beta-Endorphin release occurs during and after exercise; patients with asymptomatic ischemia had higher plasma beta-endorphin levels than did patients with symptomatic ischemia, especially during exercise. With naloxone treatment, the pain threshold of patients with silent myocardial ischemia (SMI) can be reduced to the same values as those of symptomatic patients. This supports the possibility of a role for endorphins in SMI. Patients who experience both asymptomatic and symptomatic ischemic episodes do so because their pain threshold and endorphin regulatory system varies throughout the day and because severity and duration of ischemic episodes are different. Although there is controversy over the appropriate therapy for SMI, it is more likely that this should simply be treated in the same way as painful ischemia.

Biomechanical Phenomena↗
PubMed1989

[Silent myocardial ischemia].

As an introduction the main aspects concerning clinical picture, subgroups, pathophysiology, frequency, prevalence and incidence, diagnosis, prognosis and therapy of silent ischemia are summarized: 1) CLINICAL PICTURE: Transient silent ischemia (SMI), silent infarction, relationship to sudden cardiac death, ischemic "cardiomyopathy". 2) Subgroups of SMI: SMI patients (always symptomatic patients without myocardial infarction, after infarction, after stable or unstable angina pectoris, after coronary angioplasty, and after bypass surgery). SMI episodes in otherwise symptomatic patients with coronary heart disease (without myocardial infarction, after infarction, with stable or unstable angina, after coronary angioplasty and after bypass surgery). 3) PATHOPHYSIOLOGY: SMI patients: generally reduced sensitivity to pain. SMI episodes: differences in severity and duration of ischemia. 4) Frequency: Approximately one-third of all provoked ischemic episodes are silent (independent of the mode of provocation and the ischemia indicators used), two-thirds of all spontaneous ischemic episodes are silent. 5) Prevalence and incidence: 2-5% of all healthy males aged 40-59, and 20-30% of all postinfarction patients are SMI-patients; 60-90% of all symptomatic patients with coronary heart disease have additional SMI-episodes. 6) DIAGNOSIS: screening by means of exercise ECG in patients at high risk for coronary heart disease, and in patients working in specific professions (like busdrivers, pilots, etc.). Systematic screening in postinfarction patients, in patients after unstable angina, after coronary angioplasty or bypass surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1988

ST segment monitoring before, three weeks and six months after aortocoronary bypass surgery.

ST segment monitoring by Holter ECG was conducted in 80 consecutive patients 2-4 weeks before aortocoronary bypass surgery and three weeks and six months after surgery. Preoperatively, all patients were under maximal medical therapy. In 31 out of 80 patients medical therapy could be stopped and thus 24-h ST monitoring could also be conducted without medication. Preoperative and early postoperative (three weeks) examinations were performed under hospital conditions. At 6 months after surgery the patients were monitored at home during their everyday activities. Twenty-eight per cent of patients waiting for aortocoronary bypass surgery under full medication showed transient ischaemic episodes in 24-h Holter ECG. Seventy-eight per cent of these episodes were asymptomatic. Without medication, 55% of patients had transient ischaemia. The exercise ECG data partly predicted the Holter ECG data. Patients with ST segment depression greater than 0.1 mV during exercise ECG had on Holter monitoring more and longer lasting ischaemic episodes than those with ST segment depression less than or equal to 0.1 mV. In patients with asymptomatic ST segment depression during exercise ECG the relation of silent episodes to symptomatic episodes on Holter monitoring was 5.3:1 while in patients with symptomatic ST segment depression during exercise ECG this relation was 2.3:1. Three weeks after operation the informative value of the Holter ECG was very restricted due to changes in the resting ECG caused by the operation and because patients do not exert themselves much at this time. Six months after surgery, Holter ECG is more informative, especially when conducted at home.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Bypass↗
PubMed1988

Effect of physical exercise on pain thresholds and plasma beta-endorphins in patients with silent and symptomatic myocardial ischaemia.

In a double-blind study, eight patients with symptomatic myocardial ischaemia and nine with asymptomatic myocardial ischaemia were compared during physical exercise under naloxone (6 mg i.v.) or placebo. Plasma beta-endorphin, cortisol and catecholamines were measured before exercise, during maximal exercise, and 10, 20 and 60 min after exercise. A tourniquet pain test (on the forearm, under control of transcutaneous PO2), and an electrical pain test (intracutaneous electrode placed in the finger with the electrical stimulus under computer control and two-interval forced-choice psychophysical technique) were performed before exercise as well as immediately after, and 60 min after exercise. Plasma beta-endorphin levels increased significantly (P less than 0.01) during exercise in symptomatic and asymptomatic patient groups; every patient showed an increase on beta-endorphins during and after exercise. However, the increase found in beta-endorphins during and after exercise was significantly larger (P less than 0.01) in asymptomatic than in symptomatic patients. After naloxone, this difference was no longer evident. Angina pectoris during exercise was reported with less latency in symptomatic patients (P less than 0.05) and occurred in two of nine asymptomatic patients following naloxone. The time course of plasma cortisol levels exhibited the same pattern as beta-endorphins with the same significant differences between symptomatic and asymptomatic groups. Electrical pain thresholds, though on average higher in asymptomatic patients (2.21 mA vs. 0.79 mA), were not affected by exercise or naloxone. Asymptomatic patients required more time to reach pain thresholds in the tourniquet pain test (P less than 0.02). After exercise, tourniquet pain thresholds were significantly lower (P less than 0.01) under naloxone compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1988

[Pain perception and peripheral pain localization in angina pectoris].

Cardiac nociceptive afferences are mainly transmitted by sympathetic nervous tracts. After passing the ganglion stellatum and neighbouring ganglia, the nerves enter the dorsal horn of the spinal cord at C8-Th9 (especially Th2-Th6). Here the nerve synapses for the first time, mainly to neurons which run up to the thalamus contralaterally by the tractus spinothalamicus. Apart from atypically localised pain (jaw, head, neck), the nervus vagus is rarely involved in transmitting angina pectoris pain. There is no close relation between peripheral pain localisation and localisation of coronary stenosis or myocardial ischemia areas. The localisation of angina pectoris is decided by viscero-somatic summation (convergence-projection-theory). Almost all the ascending tracts of the tractus spinothalamicus with visceral inflow also receive inflow from somatic afferences, from skin areas of the dermatome from the same segment level, and especially from deep somatic structures such as muscle and ligaments (Head's zones). Additional reflex mechanisms, where the efferent part is probably sympathetic, explain transferred effects in the matching dermatome such as hypothermic skin zones, cutaneous hyperalgesia, higher pressure sensitivity of the muscles and occasionally even dystrophic changes. The amount of spinal visceral afferences is relatively small (only 1.5-2.5% of all somatic spinal afferences). The low amount, the pronounced divergence and, compared to converging somatic afferences, the larger receptive fields in the organ explain the diffuse, barely localisable character of angina pectoris pain. Cardiac afferences are tonically and phasically inhibited at spinal and supraspinal levels, especially by descending tracts. This explains why angina pectoris can be missing in spite of pronounced peripheral nociceptive impulse rates. Patients with silent myocardial ischemia have a higher central pain threshold than patients with symptomatic myocardial ischemia. Endogenous opioids are involved in the body's own analgesia system. The beta-endorphin level in the serum rises significantly in many patients during exercise diagnostic tests. Patients with silent myocardial ischemia have higher beta-endorphin levels compared to symptomatic patients at the same exercise level. This can be interpreted as expressing quantitative differences in a superior pain regulation system. Myocardial ischemia is experienced as angina pectoris pain when the peripheral nociceptive impulse rate is so pronounced that the prevailing inhibitory pain threshold can be overcome and when the pain pathways are intact.

Angina Pectoris↗
PubMed1987

Psychophysiological mechanisms in silent myocardial ischaemia.

Six levels of coronary pain are defined and for each of them explanations for absence of pain in asymptomatic myocardial ischaemia are given: Level I: Myocardial ischaemia which can be less pronounced in amount during asymptomatic episodes. Level II: Adequate stimulus (chemical, mechanical) where biosynthesis of algogesic substances, degree of local mechanical involvement and spatial distribution may be different. Level III: For neuronal encoding the intensity theory is mainly for coronary pain, presupposing a central pain threshold which is higher in asymptomatic patients. Level IV: Conduction of painful information may be interrupted by destruction of afferent nerve ways. Level V: Spinal transmission: resting tone and ability to activate neural and humoral (endorphinergic) pain inhibition systems are stronger in asymptomatic patients. Level VI: Central processing: cognitive mechanisms (coping style) affect perception of coronary pain with differences in symptomatic and silent myocardial ischaemia.

Coronary Disease↗
PubMed1987

[Pathophysiology of painful and silent myocardial ischemia].

Regardless of the factor assumed responsible for precipitation of myocardial ischemia - varying from coronary occlusion in acute myocardial infarction to increased oxygen demand in exertional angina pectoris and reduced myocardial oxygen supply due to plaque rupture or changes in vasomotor tone in unstable angina - its incurrence may or may not be associated with pain. In the vast majority of cases, silent myocardial ischemia is observed in patients with established symptomatic coronary artery disease. Interindividual comparisons have not enabled reliable differentiation between those with painful and those with silent ischemia based on the anatomic extent of coronary artery disease, left ventricular function or previous myocardial infarction. Similarly, functional parameters such as exercise capacity, exercise duration, time to onset of ST-segment depression during exercise as well as heart rate and blood pressure both at rest and during exercise have failed to reveal differences between the symptomatic and the asymptomatic patients. Intraindividual differences have also been noted, but not consistently corroborated, and postulated as responsible for the fact that ischemia in a given patient alternates in its presence with and without pain. Since most patients with silent ischemia either have, or at some time in the past have experienced, painful ischemia, the integrity of the appropriate nervous system function can be assumed to be intact and neurocardiologic factors seem most likely to account for apparent discrepancies in pain perception. Prior to precipitation of pain, myocardial ischemia must elicit an adequate stimulus. According to some investigators, the adequate stimulus is that associated with a duration of the ischemic episode of at least three minutes and with increase in left ventricular filling pressure of more than 7 mm Hg. This threshold, consequently, represents a prerequisite but not invariably sufficient criteria for the occurrence of pain. The next step in the sequence of pain is generation of an action potential, that is, transduction by means of chemical or mechanical stimuli. During this process, a latency of 20 to 40 seconds is incurred such that the appearance of pain usually has its onset after derangement of relaxation and contraction, increased filling pressure and the observation of ECG changes. Through conduction, the information is forwarded to the central nervous system after coding of the details with regard to intensity. The intensity, in turn, is determined by the number of receptors (free nerve endings) in the field activated by the ischemic event.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris↗
PubMed1983

Experimental pain measurement in patients with asymptomatic myocardial ischemia.

Men with substantial coronary heart disease determined angiographically and with reproducible myocardial ischemia were studied. During exercise electrocardiography, 22 patients exhibited significant ST segment depression with concomitant angina pectoris (that is, symptomatic myocardial ischemia) and 20 patients demonstrated significant ST segment depression without any symptoms (that is, asymptomatic myocardial ischemia). No significant differences were found between the patient groups in functional variables, coronary angiographic data or coronary risk factors. In contrast, various experimental pain measures (for example, electrical pain threshold, according to Notermans' method, cold pressor test and tourniquet pain test) yielded significant differences between groups. Results indicate that patients with asymptomatic myocardial ischemia demonstrated significantly higher electrical pain thresholds and ischemic pain thresholds, as well as more tolerance to cold and ischemia, so that individual differences in sensibility to pain may partly explain lack of pain in patients with asymptomatic myocardial ischemia.

Angiography↗
PubMed1981

Results of exercise tests and prognosis in postinfarction patients below age 40.

In a follow-up study (mean = 3.6 years) of 555 men under 40 years of age (mean = 35.7 years) who had recently suffered transmural myocardial infarction, 44 patients (7.9%) suffered cardiac death with an annual rate of 2.2%. In a bivariate analysis a significant correlation was found between cardiac death and work capacity (p less than 0.02), vessel involvement (greater than 50% stenosis), left ventricular impairment as evaluated by ventriculography (p less than 0.001) and heart volume enlargement (p less than 0.01). There was no significant correlation between the degree of ST-segment depression and ventricular premature depolarisation (during exercise test). Complex results from non-invasive approaches can identify groups with good and bad prognosis as effectively as invasive techniques.

Adult↗