Biomedical subjects

M Kofflard

Publications and source records attributed to M Kofflard.

6 recordsLinked to original sources

PubMed1999

Spontaneous dissections of all three coronary arteries in a 33-week-pregnant woman.

The clinical course and angiographic follow-up of a woman with spontaneous coronary dissections in all three coronary arteries during the third trimester of pregnancy is described. Mother and child survived and subsequent clinical course was uneventful. At 6-month follow-up, dissections in the right and circumflex coronary artery had healed completely. At the site of the dissection in the LAD, an aneurysm had formed. This is to our knowledge the first report of antepartum and antemortem diagnosis of pregnancy related coronary dissections in all three coronary arteries. Cathet. Cardiovasc. Intervent. 48:207-210, 1999.

Adult↗

PubMed1998

[Coronary stenosis following successful radiotherapy for Hodgkin disease].

Three male patients, aged 43, 41 and 44 years, were referred to the cardiologist because of complaints of angina pectoris; one of them also had an aortic valve stenosis. Nine to 22 years before, they had received radiotherapy on the mediastinum because of Hodgkin's disease. Coronary angiography showed severe stenoses of the ostium of the right coronary artery or of the main left coronary artery, following which the patients were treated with coronary artery bypass surgery, aortic valve replacement and (or) drugs. These locations are very unusual in patients with angina who did not receive any radiation therapy, but they are seen frequently in patients who have received radiotherapy on the mediastinum. The pathogenesis of these lesions is not exactly known. The normal risk factors for atherosclerosis plus free oxygen radicals are probably involved. The free oxygen radicals, generated by radiation, locally activate coagulation via various hypothetical mechanisms. The damaging effect of radiotherapy could therefore be prevented by antioxidants. However, the therapeutic effect of radiation would most likely decrease as well. A more rational approach to prevent these vascular lesions would be to reduce the radiation load, to treat the risk factors for atherosclerosis and to give platelet aggregation inhibitors such as acetylsalicylic acid.

Adult↗

PubMed1996

Association of plasma fibrinogen levels with coronary artery disease, smoking and inflammatory markers.

The plasma level of fibrinogen is associated with the risk of ischaemic heart disease (IHD) and the severity of atherosclerosis. It has been suggested that an increased plasma level of fibrinogen is a coronary risk indicator because it reflects the inflammatory condition of the vascular wall. An inflamed vascular wall may increase the production of the cytokines interleukin 6 (IL6), interleukin 1-beta (IL1-beta), and tumour necrosis factor alpha(TNF-alpha), which have a major role in the regulation of synthesis in the liver of acute phase proteins, including fibrinogen. Smoking has also been reported to increase the levels of fibrinogen and C-reactive protein (CRP). This may indicate that smoking induces an inflammatory reaction, probably of the pulmonary bronchi and alveolae. Therefore, we anticipated that with both types of inflammation the levels of acute phase proteins and cytokines would be related. We have investigated the contribution of inflammation to the plasma levels of fibrinogen in 34 patients with severe coronary artery disease (CAD) and 30 healthy controls comparable for age and smoking habits. We did not find a parallel in the effects of smoking and ischaemic heart disease on the plasma levels of fibrinogen, CRP, IL6, IL1-beta and TNF-alpha. Cardiovascular disease had its most important effect on the plasma fibrinogen level, while smoking appeared to increase the CRP levels, while both CAD and smoking seemed to affect the IL6 levels. Our results indicate that both smoking and CAD induce an inflammatory condition but that the increase of plasma levels of different inflammatory markers is complex. Although the acute phase reaction is the main regulatory mechanism of fibrinogen, the increase of fibrinogen in our group of CAD patients could not be fully explained by increased inflammation.

Acute-Phase Reaction↗

PubMed1995

Late lumen loss after coronary angioplasty is associated with the activation status of circulating phagocytes before treatment.

BACKGROUND: The purpose of this pilot study was to identify biological risk factors for restenosis after percutaneous transluminal coronary angioplasty (PTCA) to predict the long-term outcome of PTCA before treatment. METHODS AND RESULTS: To investigate whether blood granulocytes and monocytes could determine luminal renarrowing after PTCA, several characteristics of these phagocytes were assessed before angioplasty in 32 patients who underwent PTCA of one coronary artery and who had repeat angiograms at 6-month follow-up. The plasma levels of interleukin (IL)-1 beta, tumor necrosis factor-alpha, IL-6, fibrinogen, C-reactive protein, and lipoprotein(a) before angioplasty were assessed as well. We found that the expression of the membrane antigens CD64, CD66, and CD67 by granulocytes was inversely associated with the luminal renarrowing normalized for vessel size (relative loss) at 6 months after PTCA, while the production of IL-1 beta by stimulated monocytes was positively associated with the relative loss. Next, these univariate predictors were corrected for the established clinical risk factors of dilation of the left anterior descending coronary artery and current smoking, which were statistically significant classic predictors in our patient group. Only the expression of CD67 did not predict late lumen loss independent of these established clinical risk factors. Multiple linear regression analysis showed that luminal renarrowing could be predicted reliably (R2 = .65; P < .0001) in this patient group on the basis of the vessel dilated and only two biological risk factors that reflect the activation status of blood phagocytes, ie, the expression of CD66 by granulocytes and the production of IL-1 beta by stimulated monocytes. CONCLUSIONS: The results of the present study indicate that activated blood granulocytes prevent luminal renarrowing after PTCA, while activated blood monocytes promote late lumen loss. To validate this new finding, further study in an independent patient group is required.

Angina Pectoris↗

PubMed1988

Differential bipolar sensing of a dual chamber pacemaker.

Differential bipolar sensing was evaluated in 10 consecutive patients with symptomatic heart block managed with dual chamber pacing. During pacemaker implantation atrial and ventricular electrograms were recorded using unipolar (UP) and differential bipolar (DBP) sensing amplifiers. The mean peak-to-peak amplitudes of the UP and DBP atrial electrograms were 3.3 +/- 1.2 mV and 4.2 +/- 1.2 mV, respectively. The difference was statistically significant (p less than 0.05). The mean peak-to-peak amplitudes of the ventricular electrograms were, respectively, 6.8 +/- 1.5 mV and 7.5 +/- 1.4 mV (p less than 0.01). Within 6 weeks after pacemaker implantation, patients visited the outpatient clinic. Isometric exercise tests were performed during UP and DBP sensing of the pacing system. Myopotential sensing in the ventricle occurred in nine patients during UP sensing and in none of the patients during DBP sensing (p less than 0.01) at a sensitivity setting of 0.5 mV. In addition, chest wall stimulation was performed to assess the effects of far-field signals on the ventricular sensing circuit of the pulse generator. Chest wall stimuli inhibited ventricular output during UP sensing in all 10 patients, whereas during DBP sensing inhibition of the ventricular channel occurred in three patients and then only at high output (greater than 8 V) settings. The susceptibility of the pacing system to crosstalk was also determined. However, neither during UP sensing nor during DBP sensing could cross-stimulation or cross-inhibition be demonstrated. In conclusion, DBP sensing is superior to UP sensing in terms of myopotential and far-field sensing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

Reflex cardiac asystole.

In this report we present the case of a patient with recurrent syncopal episodes. During one of the attacks the patient was monitored by telemetry and the ECG lead showed asystole for more than 7 seconds. As in cases of the cardioinhibitory type of hypersensitive carotid sinus syndrome (HCSS), asystole may represent suppression of the sinus node or suppression of both sinus and atrioventricular (AV) node. Unfortunately, in contrast to HCSS, there is no maneuver that can reproducibly induce episodes of asystole. Consequently, very little is known about the occurrence of AV block in the presence of sinus arrest. In the patient described in this report, we were able to demonstrate that suppression of sinus and AV nodes occurred simultaneously. It is interesting to note that in this type of syncope data from noninvasive and invasive techniques in assessing sinus nodal and AV nodal conduction may not be conclusive. In the group of patients with this type of syncope, permanent atrial demand pacing is contraindicated.

Arrhythmias, Cardiac↗