Twelve anesthetized mongrel dogs were subjected to systemic hypothermia and potassium-induced cardioplegia for 60 minutes with or without magnesium-1-aspartate. The effect of magnesium was assessed by indices of mitochondrial oxidative phosphorylation. Cardiac arrest was induced by potassium (20 mEq per liter) (6 dogs) or potassium (20 mEq per liter)-magnesium (8 mM per liter). The heart was reperfused for ten minutes following arrest. Dogs were supported by standard cardiopulmonary bypass with hypothermia at 20°C of myocardial temperature. Mitochondria were isolated from the endocardium, the epicardium of the left ventricle and the ventricular septum. ADP : 0 ratio state 3 respiration were well maintained in both groups following 60 minutes of ischemic arrest and 10 minutes of reperfusion. Magnesium suppressed the non-phosphorylated oxygen consumption of mitochondria, therefore, respiratory control index was significantly enhanced in the group of potassium-magnesium-1-aspartate cardioplegia. These data suggest that magnesium protects functional capacity of mitochondrial phosphorylation in the myocardium from ischemia.

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Clinical features of 19 cases with congenital aneurysm of the right sinus of Valsalva rupturing into the right ventricular outflow region (Type 1) were analysed in relation to their pathoanatomic lesions and hemodynamic alterations. Sixteen cases were operated with one surgical death. All were catheterized together with ascending aortographic study. Rupture of the aneurysm in many cases was silent or symptomless and progressive heart failure was not quite common. Symptomatology of the patients did not seem to be related entirely to status of the pathoanatomical lesions or hemodynamic alterations. Time of the rupture, and inherent right ventricular characteristics, tolerating volume overload rather well, might be, in part, responsible for its better prognosis in some cases. However, all patients with ruptured aneurysm of the sinus of Valsalva should be treated surgically. Bacterial endocarditis is a serious complication leading to death.

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In order to evaluate the histological changes in endomyocardial biopsies from 121 patients with idiopathic cardiomyopathy, quantitation of histological findings was performed and analysed by univariate and multivariate statistical analysis. Several findings, i.e. (1) disarray of myofibers, (2) hypertrophy of myofibers, (3) scarcity of myofibrils, (4) nuclear changes, (5) vacuolization, (6) proliferation of collagen fibers, (7) endocardial thickening, (8) interstitial edema, (9) cell infiltration, (10) fatty infiltration and (11) basophile degeneration, were graded in five degrees (- to 4+) or two degrees (- or +) depending upon the severity and the extent of each finding. The univariate analysis of the graded histological findings revealed no remarkable difference between the biopsies from HCM and CCM pts, except for nuclear changes, which appeared to be more prevalent in CCM (p < 0.05). In the categorical principal component analysis of the first six histological findings listed above, three principal components could be extracted. The first principal component was characterized by all six histological findings, the second by vacuolization and proliferation of collagen fibers, and the third by hypertrophy of myofibers. The mean values of the first principal scores indicated that, in either LVB or RVB histological changes were more severe in CCM than in HCM, and in fatal cases than in survivors. The second principal scores indicated that fatal cases had more collagenosis but less severe vacuolization than survivors. The histological findings in RVB appeared to be significantly correlated (r =0.41, p < 0.05) with those in LVB obtained from the same heart, but some differences were noted, myofiber hypertrophy and vacuolization being more prominent in LVB than in RVB.

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Changes in endocrine activity in response to tilting of the body were studied in 16 in-patients with various degrees of chronic congestive heart failure and one healthy subject. Norepinephrine and epinephrine excretion, plasma renin activity and plasma cortisol concentration were determined first in recumbency and then during 45 degree head-up tilting. The subjects were divided into three groups depending on the severity of heart failure. In recumbency urinary norepinephrine averaged 31.6 (standard deviation 12.7) ng/min in group 1 (controls), 54.9 ± 25.3 ng/min in group 2 (NYHA class II-III) and 79.5 ng/min in group 3 (NYHA class IV). Thus the level of urinary norepinephrine increased with the degree of heart failure. In recumbency epinephrine excretion and plasma cortisol concentration were not different among three groups. Plasma renin activity was elevated in group 3. There was a significant positive correlation between the changes in plasma renin activity and epinephrine excretion (r=0.67, p < 0.01). The present study revealed that patients with slight to moderate congestive heart failure have a normal endocrine response to tilting while those in severe failure have only a slight response. It is probable that the augmented sympathetic nerve activity and increased circulating blood volume, already present in severe failure, allow for less hemodynamic change upon tilting.

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Simulation by a digital computer of excitation spread in a human ventricular model produced displays of body surface isopotential maps. Localization of model myocardial infarctions to non-transmural and transmural sites produced distinctive differences in these displayed isopotential maps. The body surface directly over the infarcted lesion was negative in potential only in the first half period of the QRS complex and then became positive. The model demonstrated that this later positive potential was due to delayed arrival of excitation to the subepicardial layer outside of the subendocardial lesion. While, in transmural infarction, the overlying body surface remained negative in potential throughout the QRS complex. It is expectd that body surface isopotential maps will become clinically available and will permit helpful differential diagnoses between non-transmural and transmural myocardial infarctions.

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A point-score system made from symptoms, electrocardiographic findings, auscultation, and chest X-ray has been presented for the differential diagnosis among congestive cardiomyopathy, hypertrophic cardiomyopathy and ischemic heart disease. This system involved a multivariate analysis of 188 cases in which the diagnoses were established by typical echocardiographic findings, invasive examinations or autopsies. The accuracy of diagnosis by this point-score system was 91.5%. This point-score system appears to be useful as a screening test in differentiating idiopathic cardiomyopathy from ischemic heart disease.

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Drug resistant ventricular premature contractions (VPCs) in a 35-yr-old woman were successfully controlled with a contraceptive agent containing estrogen-progesterone. The VPCs in this patient always showed an R on T phenomenon resulting in occasional short run of ventricular tachycardia. Apart from the VPCs, her ECG exhibited no abnormalities. The family history revealed 9 instances of sudden unexpected death over 3 generations. The findings of myocardial biopsy of the right ventricular endocardium were characteristic of cardiomyopathy. This report discusses the possibility that a contraceptive agent successfully suppressed VPCs in a particular woman who showed a close relation between a certain period of her menstrual cycle and the occurrence of VPCs.

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When a large left ventricular aneurysm or infarct is excised, a frequent complication is inability of the left ventricle to regain adequate performance. Reduction in ventricular volume and impairment of myocardial contractility, either of which can diminish cardiac output to levels incompatible with life, are probably the main factors that lead to left ventricular failure after such surgery. A prototype prosthetic myocardium, designed to mimic the actions of the left ventricular myocardium, offers a direct means of restoring both ventricular volume and contractility after excision of a large portion of the left ventricle. In dog experiments 17 ± 1.1 % (AV ± SE) of the left ventricle was infarcted and excised under cardiopulmonary bypass. The prosthetic myocardium was implanted and activated, and changes in hemodynamic parameters produced by the assist device were studied. "On" to "off" changes in 11 dogs in congestive failure averaged over the course of the experiment were as follows : m-AoP was increased 19 ± 1.7% (Mean ± SE) : LV Syst. Press. was increased 24 ± 1.7% ; SV was increased 34 ± 3.2%, LVEDP and m-LAP were reduced 43 ± 2.4% and 22 ± 1.4% respectively ; and LVSW increased 88 ± 8.8%. With these hemodynamic benefits this prototype represents an encouraging step toward the development of a device for orthotopic replacement of damaged myocardium.

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