Effects of nifedipine after intravenous and intracoronary administration.
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Biomedical subjects
Publications and source records attributed to G Kober.
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Twenty-two patients with hypertrophic obstructive cardiomyopathy were treated with the calcium inhibitor, verapamil, which was administered in a mean oral dose of 480 mg per day. After an average of 15 months of treatment (4 to 24 months), the QRS amplitude in the electrocardiogram was significantly reduced from 4.2 to 3.8 mV. Heart volume calculated from chest x-ray films in the supine position decreased significantly from 858 to 766 ml per 1.73 m2. In 10 patients, follow-up heart catheterisation showed a decrease in left ventricular muscle mass in 7 patients and a slight increase in 3 patients. Coronary artery diameter decreased in 7 patients, increased in 1, and was unchanged in 2. The reduction in coronary artery diameter is considered to be a consequence of a reduced heart muscle mass. From all available clinical data it is concluded that verapamil treatment is superior to beta-blocker therapy.
Patients with patent coronary bypass grafts showed the followings: 1. a decrease in prestenotic coronary diameter due to a reduction in flow. 2. An increase of the poststenotic segment of the bypassed vessel due to an increase in flow via the venous graft. 3. An increase of the bypassed stenosis, mainly due to a general decrease of vessel diameter proximal to the stenosis. 4. No change in diameter in non bypassed arteries. The postoperative changes in diameter were not dependent on the time elapsed since surgery and were independent from the severity of coronary sclerosis and the number of risk factors. A correlation was found between the amount of the diameter changes and the amount of reduction in exercise induced ST-segment depression. The decrease in coronary diameter proximal to the stenosis is not due to progression of coronary sclerosis but to a functional change. A narrow poststenotic vessel does not constitute a contraindication for bypass grafting because its true diameter is flow dependent and cannot be judged with certainty from the preoperative angiogram.
During cardiac angiography the scatter radiation can reach a relevant dose at the head of the examiner. Radiation was measured with a dosimeter in the left temporal region with and without a new flexible lead-shield. The shield did not disturb the procedure. Scatter radiation was reduced to one fifth of the values without shield.
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Refering to a case report of five patients with atrial myxoma the symptoms, diagnosis, and therapy of this disease were described. In one case a biatrial tumor was found. In four cases atrial myxoma imitated a mitral-valve disease. An elevated BSR was found in all patients. The non invasive diagnostic procedure of ultrasound-echocardiography led in the last two cases to the correct diagnosis before heart-catheterization. The diagnosis was ascertained in all cases by angiocardiography. If left atrial tumor is suspected transpulmonary laevocardiography can be considered as a save diagnostic procedure better than the direct injection into the left atrium after transseptal puncture. Even the left ventricular angiogram in right anterior oblique position led in four of the five cases to the diagnosis of left atrial tumor. Coronary-angiography was performed in three patients and revealed pathologic atrial vessels in all three cases. Immediate operation is the indicated therapy. Two of the five patients were reviewed over a eight year period after operation without any signs of recurrence of the tumor.
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In 9 patients with coronary heart disease isovolumetric contractility indices and ejection phase parameters were measured simultaneously, using an angiographic catheter with a manometer at the tip (Millar). Regional wall motion at rest, after leg raising and during physical exercise (bicycle ergometer) was analyzed applying the hemiaxis method. Five weeks after aortocoronary bypass surgery the same examinations were repeated. Preoperatively left ventricular enddiastolic pressure (LVEDP) increased from 21 to 37 mm Hg following leg raising. The velocity mean of fiber shortening (Vcf) and of regional fiber shortening in the anterior wall decreased significantly.--All patients discontinued physical exercise due to angina pectoris. LVEDP increased from 21 to 39 mm Hg. Large hypokinetic and akinetic areas developed especially in the anterior wall. Velocity of fiber shortening of the anterior wall decreased from 1.43 to 0.76/s. Enddiastolic volume remained unchanged while endsystolic volume increased significantly. In six patients with patent grafts surgery had a beneficial effect. Comparing angiograms at rest no significant changes were found. After leg raising and physical exercise, however, marked improvement in ventricular function occurred, compared to the preoperative performance. All 6 patients were exercised without complaints at a load of 100 watts for 8 minutes. Velocity of fiber shortening in the anterior wall increased significantly from 0.76 to 2.56/s, mean Vcf from 1.11 to 2.12 circ/s, max dP/dt from 2302 to 4280 mm Hg/s and Vpm from 27.8 to 55.7/s. Functional improvement in individual wall segments amounted to 500% in the mean. Ejection fraction increased from 54 to 76%. Enddiastolic volume remained unchanged while endsystolic volume decreased from 67 to 33 ml/1.37 m2 (p less than 0.002). In three patients the bypass occluded or myocardial infarction occurred intraoperatively. Postoperative findings at rest and during exercise were unchanged as compared to preoperative values. Following successful bypass surgery ventricular function at rest did not change. During exercise, however, a marked improvement in overall and in regional ventricular function was found.
In 16 patients with coronary heart disease (n = 13) and cardiomyopathy (n = 3) heart rate, left ventricular pressure and contractility (max dp/dt, min dp/dt and Vpm) were measured prior during and after three consecutive left ventricular angiograms. Heart rate decreased during angiography and increased slightly but significantly after angiography. Systolic and diastolic left ventricular pressure, max dp/dt and min dp/dt increased after angiography, whereas Vpm remained unchanged. Any hemodynamic changes occuring were moderate and only of short duration. No significant differences were found a) between patients with angiographically proven normal and reduced left ventricular function, b) between patients with normal or increased left ventricular filling pressure or c) between those with slight or severe coronary heart disease. The investigations point to a good tolerance for the sodium methyl glucamine salt of diatrizoic acid (Urografin 76) even in patients with progressed coronary heart disease. Severe side-effects described in animal experiments indicate a poor comparibility between animal models and human studies. Moreover animal experiments are mostly done with high doses not used clinically.
The serum and total body potassium was investigated in 25 patients with non-congestive cardaic failure before and during saluretic treatment. Treatment with triamterene (100 mg/d; n = 10) over a period of 3 weeks led to an increase of serum potassium (from 4.1 +/- 0.65 to 4.7 +/- 0.51 mmol/l) and of total body potassium (by 110 mmol). After treatment with chlortalidon for 7 days (100 mg/d; n = 6) serum potassium concentration decreased from 4.38 "/- 0.37 to 3.30 +/- 0.46 mmol/l (approximately 25%). The total body potassium decreased by 240 mmol (approximately 10%). Continuation of the treatment with a combination of chlortalidon (50 mg/d) and triamterene (150 mg/d) led to correction of the extra- and intracellular potassium loss after 1 to 2 weeks. No significant change of serum and total body potassium was found during and after 6 months of treatment with hydrochlorothiazide (50 mg/d) and triamterene (100 mg/d; n = 9). The results demonstrate the potassium loss which occurs in the early stage of saluretic treatment and show the antikaluretic potency of triamterene.
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Regional and overall left ventricular contraction reserve was studied in 14 patients with coronary heart disease, in 5 healthy subjects and in 4 patients before and after aorto-coronary bypass surgery. Quantification of overall contraction was based on ventricular volumes and ejection fraction. Regional contraction reserve was calculated with the hemiaxis method and a ventricular score. Contraction reserve under nitroglycerin and in postextrasystolic beats was compared. For routine quantification of contraction reserve the ventricular score is recommended. For research purposes the hemiaxis method is to be preferred. Postextrasystolic beats are better suited for analysis of contraction reserve than are angiograms following administration of nitroglycerin. This is due to the minor expense of the procedure, furthermore, postextrasystolic beats allow better differentiation between contracting and non-contracting areas. Left ventricular contraction reserve is larger in patients with coronary heart disease, angina pectoris and ischemic reactions in the exercise ECG than in control patients. These findings are based on overall and on regional volume parameters. A quantitatively greater improvement in contraction could be provoked in the anterior wall than in the posterior wall. Regional contraction improved significantly in most cases either in the anterior wall or in the posterior wall; rarely it improved simultaneously in both left ventricular regions. In a few cases contraction deteriorated in one area with a simultaneous improvement in the opposite area. Overall and regional ventricular function, as assessed preoperatively by contraction reserve determinations could not be completely regained in normal beats after successful bypass surgery. Differences in the regional contraction reserve seemed to be mainly due to varying degrees of ischemia and scarring.
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In 41 patients with different types of cardiomyopathy (19 congestive = COCM, 6 hypertrophic obstructive = HOCM, and 16 hypertrophic non-obstructive = HCM) ventricular enddiastolic volume (EDV), endsystolic volume (ESV), and ejection fraction (EF) were determined angiographically and values of both ventricles were compared. In the mean, volume parameters increased significantly and EF of both ventricles decreased as compared to control values of patients with coronary heart disease without myocardial infarction. In COCM volume parameters reached pathologic values as in the total patient group whereas in HOCM and in HCM values did not differ significantly from control. Left ventricular function was reduced more often and, in the mean, more severely than right ventricular function. This became evident e.g. from the incidence of enddiastolic volume increase and the course of the regression line. A similar finding can be derived from the reversal of the normal relation of volume parameters of both ventricles. Only in rare cases right ventricular function was more severely impaired than left ventricular function. These findings indicate a simultaneous impairment of both ventricles in cardiomyopathy. The more pronounced left ventricular function disturbance may be attributed to the higher left ventricular work load. Thus, left ventricular biopsies might be of greater diagnostic significance than right ventricular biopsies.
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In 17 mainly coronary patients increase in blood flow due to therapeutical vasodilation was measured in the region almost totally supplied by the left coronary artery by two different methods, the 133-Xenon washout technique and via arterio-venous oxygen difference (AVDO2). With both methods similar results were obtained (r=0.89). Mean maximal increase in flow 15 min. after 40 mg Carbochromen i.v. amounted to +22.4% with the 133-Xenontechnique, +21.5% with AVDO2. 5min. after 20 mg intracoronary dipyridamol mean flow increased by 47.8% (Xenon technique) and 47.1% (AVDO2) respectively. Decrease in coronary reserve is correlated more with the amount of damaged byocardium than with the degree of coronary obstruction. The limited reliablility of all measurements of total coronary blood flow in heart diseases with regional disturbances is specially indicated.