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51 patients with primitive cardiomyopathy were studied and classified (5 groups) on the basis of hemodynamic parametres and the modalities of left ventricular contraction: the first group was made up of patients with "frontal sector" hyperkinesia, normal ejection fraction and without any dynamic obstruction of the ventricular flow; the second, of patients with hyperkinesia "frontal and rear sector" raised ejection fraction and with dynamic obstruction; the third group was composed of patients with "frontal sector" hyperkinesia, reduced motility of the mitralic valvular level with appearance of insufficiency (maintained in the subsequent groups) and depression of the ejection fraction; dynamic obstruction was present. Groups IV and V included patients with progressive extension of hypokinesia to all marginal regions, up to the contraction pattern characterized by "serious and diffused hypokinesia". To conclude, a correlation of the contraction patterns is made, characterizing the various groups with a pathophysiological interpretation.
G Ital Cardiol 1976
PMID:[Primitive cardiomyopathies: dynamic geometry of left ventricular contraction]. 101 Feb 33

Hemodynamics and myocardial muscle mechanics have been studied in 22 euthyroid and 60 hypothyroid cats in which experimental hypothyroidism has been produced by thyroidectomy 61 days prior to the examination. Left ventricular to body weight ratio was altered due to a decrease in left ventricular weight and an increase in body weight. Heart rate, cardiac output and cardiac index were decreased (by 12-15 per cent), whereas stroke volume remained unchanges. Peak systolic pressure of the left ventricle was moderately decreased, the other pressures were in the normal range. There was a marked and significant reduction of isovolumic contractility indices indicating a depression of myocardial contractility in situ by 20-27 per cent. The isolated ventricular myocardium exhibited decreases of isotonic muscle shortening, of maximum isometric tension development and of the rates of both, isotonic shortening and isometric tension development by 12-35 per cent. Force-velocity relationships of contraction and relaxation were depressed to lower values of contraction and relaxation velocity as well as of maximum isometric muscle tension. The alterations in myocardial muscle mechanics and hemodynamics were completely reversible following substitution of the hypothyroid group with physiological doses of L-thyroxine (5 mug/kg/day for 8-18 days). Excess increases of parameters of myocardial performance were found following substitution of the hypothyroid group with L-thyroxine (500 mug/kg/day) in accordance with the induction of experimental hyperthyroidism in these animals. The results demonstrate impaired myocardial contractility and hemodynamics in experimental hypothyroidism. These changes are completely reversible by substitution with L-thyroxine in accordance with a reversible thyroid cardiomyopathy. The cellular mechanisms responsible for the altered cardiac activity in experimental hypothyroidism are discussed.
Basic Res Cardiol
PMID:Experimental hypothyroidism: depression of myocardial contractile function and hemodynamics and their reversibility by substitution with thyroid hormones. 101 93

The effects on myocardial function, metabolism and ultrastructure of 60 minutes of reperfusion, instituted after 30, 60 and 90 minutes of occlusion of the left anterior descending coronary artery, were studied in 48 dogs. Twelve sham-operated dogs served as controls. Coronary occlusion for 60 or 90 minutes caused significant depression in the first derivative of left ventricular pressure (dP/dt) (P less than 0.05) that could not be reversed by reperfusion. Upon reperfusion, creatine phosphate stores in myocardium made ischemic for 30 and 60 minutes, but not for 90 minutes, returned toward control levels, but stores of adenosine triphosphate (ATP) and total nucleotides and the ATP/adenosine diphosphate ratio of myocardium subjected to 60 and 90 minutes of ischemia were further decreased. After 60 and 90 minutes of ischemia, swelling of the sarcoplasmic reticulum and mitochondrial damage (swelling, decreased matrix density and partial loss of cristae) were seen. Myofibrils were relaxed in all these groups. Reperfusion produced gross contraction of myofibrils and aggravated these changes in mitochondria and sarcoplasmic reticulum. In the hearts subjected to 90 minutes of ischemia these changes were gross. The levels of creatine phosphokinase, glutamic oxaloacetic transaminase and lactic dehydrogenase in the coronary sinus blood increased dramatically (P less than 0.05) upon reperfusion after 60 or 90 minutes of occlusion, indicating severe impairment of cell membranes. This secondary rise in serum enzyme activity during reperfusion should be taken into consideration when estimating the size of a myocardial infarct from enzyme changes alone. It appears that 60 and 90 minutes of ischemia cause severe myocardial damage that is not reversed by reperfusion maintained for 1 hour although longer periods of reperfusion may be beneficial.
Am J Cardiol 1975 Aug
PMID:Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion. 108 Mar 52

The study of 46 patients with frequent anginal episodes characterized by S-T elevation (so called "variant angina pectoris") demonstrated that this type of electrocardiographic pattern does not characterize a homogeneous group of patients. In fact, while in some patients angina occurred only at rest, in others it occurred also on exercise. Sometimes ecgraphic alterations characterized by S-T depression were observed on the same leads which on other occasions had shown S-T elevation. The angiographic picture revealed: absence of significant coronary alterations in 10% of cases, stenosis greater than 75% in one main branch in 29%, in two branches in 39% and in three branches in 22% of cases. The hemodynamic monitoring carried out on 14 of these patients demonstrated that the ecgraphic modifications occur before the onset of the hemodynamic parameters which control myocardial O2 consumption. This suggests a primitive reduction of regional myocardial blood supply as a cause of the ischaemic episodes. The study of the regional myocardial perfusion with 201Tl technique in 6 patients confirmed this hypothesis. Coronary angiography carried out during an ischemic episode showed that the reduction of myocardial blood supply was caused by a spasm of a large coronary artery involving a long segment of the vessel, reversible by nitroglycerin administration. Aorto-coronary by-pass operation performed on 6 patients was followed by the disappearance of pain in two patients, even though the "by-pass" patency was angiographically proved in two patients.
G Ital Cardiol 1976
PMID:[Clinical coronarographic characteristics and pathogenetic mechanism of angina pectoris with s-t elevation (author's transl)]. 108 26

The effect of verapamil were studied on 50 episodes of supraventricular and ventricular tachycardia in 44 patients. An i.v. dose of 0.10 to 0.15 mg/kg. was used. In 5 cases His bundle electrograms were obtained while maximal dp/dt was determined in 7 others. Sinus rhythm was obtained in 21 (81%) of 26 cases of PSVT. In all cases of rapid atrial fibrillation (n-11), an important decrease in the ventricular response was elicited. Of 7 cases of atrial flutter, verapamil induced sinus rhythm in 3 and a significant decrease in the ventricular rate in 3 others. In 2 out of 6 cases ventricular tachycardia reverted to sinus rhythm. The latency time between the injection and the manifestation of the effect ranged from 2 to 4 minutes. A slight and short-lasting depression of dp/dt was observed in all cases studied. Verapamil produced an increase in the A-H interval in 4 of the 5 cases studied with His bundle recordings. Verapamil was found to be a useful drug to suppress PSVT, to decrease the ventricular response in flutter or atrial fibrillation and to convert some ventricular tachycardias to sinus rhythm. Verapamil should be used with caution in previously digitalized patients and is contraindicated when there is S-A node dysfunction as in the tachycardia-bradycardia syndrome.
Arch Inst Cardiol Mex
PMID:[Antiarrhythmic effects of verapamil]. 108 54

Sinus nodal function was analyzed in 25 dogs by premature stimulation of the right atrium. The return (AT-AR) and post-return (AR-A) cycles were plotted as a function of the premature cycle, and four zones were identified. Zone I (compensatory zone) was observed during the last 4.8 percent (mean value) of the sinus cycle (A-A). Zone II was observed during 43.6 to 95.2 percent (mean value) of the sinus cycle. During the latter part of zone II, AT-AR was nearly constant and AR-A remained nearly equal to A-A during the last 29 percent (mean value) of the cycle. Earlier in zone II three distinct patterns of return cycle responses were observed whereas post-return cycles either remained nearly equal to A-A or showed progressive lengthening. Zone III (interpolation) was observed in 10 animals during 39.5 to 46.2 percent (mean value) of the sinus cycle. AR-A was nearly equal to A-A in zone III. Interpolation was incomplete late and complete early in the zone. Zone IV (echo zone) was seen in another 10 animals during 40.9 to 45.3 percent (mean value) of the sinus cycle and in this zone AR-A was greater than A-A. No significant difference in these zones was seen among the animals anesthetized with pentobarbital or alpha-chloralose, or given 6-OH-dopamine. The AR-A was important in the analysis of these zones and appears to be essential to the interpretation of data derived from premature atrial stimulation. Responses to premature atrial stimulation through a catheter electrode positioned against the sinus nodal region compared favorably with responses to direct epicardial stimulation. After periods of continuous right atrial pacing a vairety of patterns of sinus nodal depression were observed at different rates and durations of stimulation. The frequent occurrence of a short sinus escape cycle followed by the maximal pause observed during rapid pacing rates suggests sinus nodal entrance block. This may be an important factor to consider in determining an optimal pacing rate for assessing sinus nodal function.
Am J Cardiol 1975 Apr
PMID:Sinus nodal function in the intact dog heart evaluated by premature atrial stimulation and atrial pacing. 111

Eleven elderly patients with idiopathic pericarditis are reported. All but one were older than 60 yr. Evidence of ischemic cardiovascular disease was present in 8 patients. The initial diagnosis was heart failure with pulmonary complications in 4 cases and myocardial infarction in 3. Respiratory infection preceded the onset of pericarditis in 5 cases. Presenting symptoms were typical precordial pain, fever and dyspnea. Pericardial friction was found in 7 cases and transient rhythm disturbances in 5. Four patients had ST elevation and 3 had ST depression in their electrocardiograms. Other findings included an increased sedimentation rate, leukocytosis, elevated venous pressure and normal SGOT levels. Antibiotics were of no avail but prednisone had a dramatic effect. Two patients had a relapsing course lasting 2 yr or more. One patient, who died at the age of 75 from bleeding ulcer, had patent coronary arteries and mild perimyocardial fibrosis. The diagnosis of idiopathic pericarditis in the aged is difficult because the disease simulates ischemic heart disease in patients who frequently have evidence of arteriosclerotic cardiovascular involvment.
Eur J Cardiol 1975 Jan
PMID:Acute idiopathic pericarditis in the aged. 114 70

To elucidate the determinants of the poor prognosis of patients with left main coronary artery disease and to assess the efficacy of diagnostic and therapeutic interventions the angiographic features and clinical course of 58 patients with left main coronary artery disease studied between September 1967 and June 1974 were analyzed. Eighty-three coronary arteriograms were obtained in these 58 patients using the Judkins technique; there were no immediate complications although one patient died 3 days after study. Previously cited predictors of left main coronary artery, unstable or nonexertional angina and marked S-T segment depression with exercise were found in a minority of patients; thus, the presence of the disease could not reliably be predicted before arteriographic study. Coexisting disease was found in either two or three other coronary arteries in 46 of 58 patients; only 2 patients had isolated left main coronary artery disease. Because the criteria for operability have changed in recent years, current criteria without knowledge of the treatment actually given or its outcome. The condition of 10 of 58 patients was judged inoperable in retrospect because of severe coexisting distal coronary artery disease (8 patients) or ventricular dysfunction (2 patients). Of 19 patients whose condition was judged operable in retrospect but who were treated without surgery, 9 died, 8 within 18 months; 10 have survived 12 to 83 months. Another 27 patients with a condition judged operable in retrospect had received saphenous vein bypass grafts. In this group, there were four operative and three late deaths. The severity of angina decreased in survivors treated surgically but was unchanged in survivors treated without surgery. The improvement in survival rates of surgically treated patients was not statistically significant. The data indicate that coronary arteriography can be performed at low risk with the Judkins technique even though preangiographic prediction of left main coronary artery disease is unreliable. Coexisting disease in oter major coronary arteries is an important determinant of the poor prognosis of patients with left main coronary artery disease and precludes surgery in 13 percent. Isolated left main coronary artery disease is uncommon. Surgical therapy relieves symptoms more effectively than nonsurgical therapy.
Am J Cardiol 1975 Aug
PMID:Left main coronary artery disease. Risks of angiography, importance of coexisting disease of other coronary arteries and effects of revascularization. 115 34

To study the efficacy of isosorbide dinitrate in prevention of myocardial ischemia, 20 patients with angiographically proved coronary artery disease underwent atrial pacing (mean rate 138/min) before (P1), 10 minutes after (P2) and 65 minutes after (P3) sublingual administration of 5 mg of isosorbide dinitrate. The symptomatic, hemodynamic and metabolic responses were evaluated at rest and during each pacing period. Angina occurred in all subjects during P1. Angina did not recur or was less severe in 17 of 19 patients during P2 and in 19 of 20 patients during P3. Resting left ventricular end-diastolic pressure for the group was normal at 11 plus or minus 4 mm Hg (mean plus or minus standard deviation). On interruption of pacing at 4.5 minutes during P1, average end-diastolic pressure during sinus rhythm was abnormal (18 plus or minus 6 mm Hg). After administration of isosorbide dinitrate mean left ventricular end-diastolic pressure was significantly decreased at rest and remained normal when pacing was interrupted during P2 and P3. Brachial arterial pressure, cardiac index, tension-time index, left ventricular stroke work index and maximal rate of rise of left ventricular pressure were all diminished at rest before and during P2 and P3. S-T segment depression was less during P2 and P3 than during P1. Before isosorbide dinitrate was given, resting myocardial lactate extraction was 15 plus or minus 11 percent during P1 lactate extraction decreased to minus2 plus or minus 25 percent. Lactate extraction was significantly greater during P2 and P3 than during P1. This study demonstrates that sublingual administration of 5 mg of isosorbide dinitrate has a significant protective effect against pacing-induced myocardial ischemia at 10 and 65 minutes after administration.
Am J Cardiol 1975 Aug
PMID:Effects of isosorbide dinitrate on the response to atrial pacing in coronary heart disease. 115 42

Volume manipulations in 27 patients (volume loading n = 22; phlebotomy n = 5) with acute myocardial infarction (AMI) and 7 normal subjects has been performed in order to evaluate left ventricular performance in terms of cardiac index (CI) and pulmonary artery enddiastolic pressure (EDPAP). An EDPAP in the range of 18-22 mm Hg was in general associated with maximal cardiac output. In patients with AMI maximal cardiac performance was significantly lower compared to normal subjects (p less than 0.01). Volume loading that increased the EDPAP beyond the level of 18-22 mm Hg usually deteriorated cardiac performance in AMI. A phlebotomy in 5 subjects with severe pulmonary congestion decreased EDPAP significantly from 32 to 24 mm Hg (p less than 0.1) without a change of cardiac index (2.2 - 2.5 1/min/m2;NS). In 11 patients left ventricular performance was assessed during the acute and convalescent period. 4-6 weeks after AMI resting EDPAP decreased from initially 16 to 11 mm Hg (p less than 0.02), whereas cardiac index did not change significantly (3.1-3.3. 1/min/m2;NS) and even did not rise markedly after volume loading (3.3-3.4 1/min/m2;NS). By plotting the relative change of cardiac index after volume loading against the individual infarct size (n = 16), left ventricular hemodynamic reserve was assessed and revealed a significant depression compared to normal subjects (n = 7). A rough reverse relationship (r = -0.69) between left ventricular hemodynamic reserve and infarct size was observed.
Eur J Cardiol 1975 Aug
PMID:Assessment of left ventricular function and hemodynamic reserve by volume loading in acute myocardial infarction. 118 69


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