[Percutaneous transluminal coronary angioplasty: qualifications of the physician and patient safety, logistic considerations].
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Biomedical subjects
Publications and source records attributed to P Lichtlen.
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In 173 women less than 50 years of age with myocardial infarction, angiographic evidence of coronary sclerosis was observed in only 108 (62%). Completely normal coronary arteries were found in 15 patients (9%) and in 50 patients (29%) an isolated poorly delineated stenosis was found in the presence of otherwise completely normal coronary arteries. Of the 65 patients with myocardial infarction but without typical coronary sclerosis, 47 (72%) were taking oral contraceptives at the time of infarction. In 60% of the oral contraceptive users with infarction, angiographically, there was no evidence of typical coronary sclerosis. With the exception of cigarette smoking, the number of atherogenic risk factors in these patients was low such that myocardial infarction during treatment with oral contraceptives may possibly represent a separate disease entity distinguishable from coronary sclerosis. In support of this, in some cases, repeat angiography demonstrated spontaneous regression of the isolated stenosis. Etiologically, possible thromboembolic vascular occlusion has been assumed. In women in the premenopausal years, coronary sclerosis is uncommon and usually associated with a substantial number of atherogenic risk factors. In this case, 29% of the women had used oral contraceptives, the causal role of which remains uncertain. Even though oral contraceptive use is associated with a higher risk of myocardial infarction, apparently, it cannot be regarded as a typical atherogenic risk factor.
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Parathyroid hormone (PTH) influences the calcium metabolism of many different mammalian cell types; indeed, hypertension due to changes in muscle tone is a frequent symptom of hypercalcemic hyperparathyroidism. In a blind study of 81 patients with various forms of heart disease undergoing coronary angiography, the plasma concentrations of the midcarboxyl regional PTH immunoreactivity were determined. PTH concentrations were elevated in 26 of the 56 patients exhibiting organic coronary artery disease (CAD). The plasma PTH levels were highest in those patients with CAD affecting three vessels and in patients with evidence of myocardial infarction. PTH levels were not influenced by previous drug treatments, and did not correlate to stress hormone levels. We propose that increased PTH levels may be a marker for initiation or potentiation of calcium-dependent changes in vascular smooth muscle behavior inducing coronary functional and anatomic lesions typical of CAD.
An overview is provided of current thinking regarding the origin(s) of atherosclerosis on the basis of clinical evidence, experimental models and pharmacological investigations with calcium antagonists. Because this group of drugs inhibits the influx of Ca2+ into the smooth muscle cell of the cardiovascular wall, it has been argued that when endothelial damage is anticipated or has occurred, the 'protective' action of calcium antagonists might avoid, delay or even help to repair the calcium overload seen with cell membrane damage. In the real world the situation must be far more complex as will become evident but as a concept the avoidance of Ca2+ overloading is enticing. In fact, based on circumstantial evidence, a major clinical trial is currently in progress in which the long term effect of nifedipine on coronary atherosclerosis is being evaluated in a double blind randomized fashion. The end-point of this study lies in the reduction of the severity and number of coronary artery lesions. Although not yet completed, the design and goals of that study are provided.
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In 36 patients with atrial flutter, atrial fibrillation or supraventricular tachycardia, refractory to medical treatment, who underwent interruption of atrioventricular conduction by means of an electrode-catheter, i.e. His bundle ablation, various pacemakers were studied. In 22 patients (group I) a heart rate programmable VVI-pacemaker was implanted, in 7 patients (group II) an activity-mode pacemaker (Activitrax 8400, Fa. Medtronic) and in 7 patients (group III) a QT-mode pacemaker (Quintech 911, Fa. Vitatron). To study physical work capacity, exercise testing was performed using a bicycle ergometer in group I and group III and a treadmill in group II. Sixteen patients with VVI-mode pacing (72.7%) complained of shortness of breath during exercise in normal daily life, in comparison to only 2 patients in group II (28.6%) and 3 patients in group III (42.9%). The exercise test revealed a normal physical work capacity in only 3 out of 22 patients (13.6%) with a VVI-pacemaker, but a normal physical work capacity in all patients with activity-mode or QT-mode pacing. Heart rate during stress test in patients with an Activitrax-pacemaker increased more rapidly than in patients with a Quintech-pacemaker and also dropped more quickly in the Activitrax-group than in the Quintech-group after cessation of the stress test. It is important to note that pacemaker reprogramming was necessary in 1 out of 7 patients (14.3%) with activity-mode pacing and in 4 out of 7 patients (57.1%) with QT-mode pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
36 patients with 68 aorto-coronary venous bypass grafts (45 of which were angiographically patent) were examined via DSA (DV12V, serial mode, Philips) and angiography. Imaging was triggered via R waves, and effected in RAO 30 degrees, LAO 60 degrees, and AP projection. 63 of the 68 grafts were correctly detected (92.7%). Two anterior interventricular branch grafts (RIVA = ramus interventricularis anterior) were not visualised via DSA (95.6% sensitivity). One graft each to the RIVA, to the right coronary artery (RCA), and to the posterior branch of the lateral cutaneous branches of intercostal arteries (PLA), were falsely found to be patent (87% specificity). Grafts were visualised in full length. In some cases morphological changes of the walls were also visible.
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The characteristics of progressive coronary artery disease as judged from sequential angiography were quantitatively analysed in 19 patients with stable angina in whom coronary angiograms were repeated after 64-104 months (average 76.5 months). The diameters of at most 15 corresponding segments were measured with a vernier caliper (accuracy: 0.05 mm) at identical sites and in the same projections. Considering the error in measurement (less than 10%) and spontaneous changes in smooth muscle tone only a diameter decrease of greater than 20% and/or every transition to an occlusion were recorded as progression. The progression over a 6-year interval was predominately characterized by: A large amount of total occlusions (61% of all progressive stenoses), relatively independent of the initial degree of stenosis. A large amount of newly developed obstructions which are more severe in coronary arteries already segmentally diseased at the onset, indicating a diffuse intramural disease of the entire vessel. A different pattern of progression in the 3 main coronary arteries. No influence of risk factors on natural history.
The natural history of coronary artery disease has to be studied by comparing coronary angiograms of the same patient taken at different times. However, conclusions from repeated angiographic studies are fraught with substantial errors mainly because of: 1. patients selection, 2. variable time interval and 3. technical pitfalls. Despite this bias published interval studies demonstrate that coronary atherosclerosis predominantly is a progressive disease: after 2-3 years 50% to 60%, after 3-4 years 60% to 70% and after 5 years more than 80% of patients demonstrate progressive coronary artery disease at angiography. In addition, quantitative evaluation of coronary angiograms reveals that progression of coronary artery disease: 1. has a variable pattern and pace in each coronary artery and 2. predominantly involves initially normal coronary artery segments. From all clinical and angiographic parameters under scrutiny progressive coronary artery disease is significantly correlated to: abnormal lipid levels at the time of the first angiogram, a period of unstable angina pectoris, interval myocardial infarction and initial severity of coronary artery obstruction. It has to be emphasized, however, that in the individual patient the speed of progression is highly variably supporting the concept of different underlying pathophysiological mechanisms (primary/secondary progression). Regression or coronary stenosis is a rare phenomenon which may occur spontaneously and is anecdotally reported in patients after vigorous treatment of severe hyperlipoproteinemia.
A new method for quantifying regional variations in extravascular lung water (rELW) has been developed. The positron source 15O (T1/2 = 2.0 min.) was provided as H215O 'on line' by constant intravenous injection. Tomographic images (PET) of the water distribution were obtained during equilibrium. The distribution of blood volume was obtained by marking erythrocytes (carboxyhaemoglobin) using a bolus inhalation [C-11)-CO; T1/2 = 20.4 min). Absorption is calculated from transmission tomography. The rELW is defined as: total lung water minus intravascular space. The method was carried out in five intubated and anaesthetised dogs before and after induction of pulmonary oedema with oleic acid (0.06 ml./kg.). Mean ELW (PET) rose from 0.13 +/- 0.02 g./cm.3 to 0.24 +/- 0.04 g./cm.3. There was good correlation with a simultaneously performed thermo-dye method (7.1 +/- 1.3 ml./kg. KG to 13.3 +/- 1.9 ml./kg. KG; r = 0.94). Gravimetric estimations resulted in 13.7 +/- 2.6 ml./kg. KG. The development and distribution of the pulmonary oedema was non-homogeneous and varied regionally.
The aim of surgical therapy for ventricular arrhythmias is to eliminate the areas of diseases myocardium from which ventricular tachycardias originate. According to the results of endocardial mapping a 2 to 3 mm deep endocardial incision is performed around the identified arrhythmogenic area. Within the past 12 months, 19 patients with coronary heart disease and complex ventricular arrhythmias were operated upon. In 16 cases an endocardial incision was performed. In 5 a left ventricular aneurysm was resected as well, 4 patients received one to 4 coronary vein grafts, and in 7 patients aneurysmectomy and bypass grafting were combined. Except for one relapse, no ventricular tachycardia has reappeared since the operation. Ventricular tachycardia could not be initiated by intracardiac stimulation postoperatively in any of the cases restudied. Four patients died from causes unrelated to ventricular arrhythmias. Direct surgical therapy was proven a promising new approach in patients with ventricular tachycardia or complex ventricular arrhythmia refractory to medical treatment. Our technique of endocardial incision appears to be effective and less traumatic to the myocardium than the original transmural encircling incision.