A B S T R A C T Human cardiac ventricular myosins were prepared from autopsy samples from nine adults, seven infants, and from surgical specimens from seven patients undergoing left ventricular septal myectomy for obstructive hypertrophic cardiomyopathy. Infant myosin differed from adult myosin in two important characteristics: (a) t-30% of the 27,000-dalton myosin light chain is replaced by a 28,000-dalton light chain, and (b) the actin-activated myosin MgATPase activity of infant myosin is significantly lower than that of adult myosin (64 nmol phosphate released/mg myosin per min vs. 124 nmol/mg per min at 37°C). The K+-EDTA ATPase activity of the myosin measured in 0.5M KC1 is also lower in infants (1,210 nmol/mg per min vs. 620 nmol/mg per min at 37°C), but the Ca++-activated ATPase is not significantly different. There were no differences in enzymatic activity between the normal adult and cardiomyopathic myosins.A detailed study was performed to investigate possible variations in the structure of the myosin heavy chain in infant, adult, and cardiomyopathic samples. There were no significant differences between infant and normal adult, or between normal adult and cardiomyopathic myosins seen in pyrophosphate polyacrylamide gel electrophoresis, or peptide mapping using alpha-chymotrypsin, papain, or cyanogen bromide to generate peptides.These results suggest that isoenzymes of human ventricular myosin do not exist for the myosin heavy chain in the specimens examined from infants, adults, and patients with obstructive hypertrophic cardiomyopaDr. Schier's present address is
To evaluate the role of selective intra-arterial low-dose thrombolytic therapy (SILDT) as an alternative to the surgical management of acute arterial occlusion, the hospital records of 40 patients who underwent 43 SILDT treatments with either streptokinase (36) or urokinase (7) between December 1979 and March 1984 were reviewed. Twenty-eight patients underwent 30 treatments (group 1) for native arterial occlusion and 12 patients underwent 13 treatments (group 2) for prosthetic or autogenous graft occlusions. Therapy was deemed successful if subsequent surgical therapy was obviated. In group 1, SILDT was successful in 13 of 28 (45%) patients with 12 of 25 lower extremity occlusions and one of three upper extremity occlusions. Successful lysis in the native artery occlusion group fell into three categories: five patients were successfully treated for arterial thrombosis complicating percutaneous transluminal angioplasty (PTA); four patients required PTA after complete lysis revealed an underlying arterial stenosis; and only three required no further therapy after SILDT. SILDT failed in all three patients with the aortoiliac occlusions. Eleven patients with femoral artery occlusions and unsuccessful SILDT required six bypass procedures, three amputations, one embolectomy, and one PTA. In group 2 only 3 of 14 treatments (21%) were successful. Bypass revision was not possible in 11 patients and all required amputation. Systemic fibrinolysis was seen in 20 (59%) of 34 patients with available data. Neither fibrinogen levels nor fibrin degradation products predicted the occurrence of complications. Minor complications occurred in 18 of 43 (43%) treatments; small hematomas at the catheter entry site were most common. Minor complications occurred in 20 of 43 treatments (44%) and included severe local hemorrhage (four), distant bleeding (three), pulmonary embolism (four), myocardial infarction (three), unmasking of an aortoduodenal fistula (one), and clot migration requiring emergency thrombectomy (four). SILDT is most effective in acute arterial thrombosis complicating arteriography or percutaneous angioplasty. It may play a role in the patient in whom thrombolysis can reveal an underlying stenosis amenable to percutaneous angioplasty. This experience shows SILDT to be of limited value in the management of prosthetic autogenous graft occlusions. Finally, thrombolytic therapy is associated with significant morbidity and mortality rates and requires cautious monitoring to detect arterial thrombus migration, worsening tissue ischemia, venous thromboembolism, intracerebral hemorrhage, and local or systemic bleeding.
Background: Previous studies in small groups of predominantly nongeriatic patients showed that complè ventricular arrhythmias occurring after coronary artery graft (CABG) surgery are of no prognostic significance. The purpose of this study was to compare the prognosis of patients with and without advanced grade ventricular arrhythmias (AGVA) after CABG in a large group of patients. [In this paper, AGVA is used as an abridged definition of frequent premature ventricular complexes (PVCs) and nonsustained ventricular tachycardia (NSVT) which represent advanced grade ventricular arrhythmias.] Methods: Twenty‐four hour ambulatory electrocardiographic (ECG) monitoring was performed 3 days after CABG in 185 consecutive patients with and 185 closely matched control patients without AGVA. Of 185 patients with AGVA, 77 had frequent PVCs, 45 had NSVT, and 63 patients had both. The average age of both groups was 65 ± 9.7 years. Patients were followed for 34 ± 10 months, and in 30 patients ambulatory monitoring was repeated at the end of the follow‐up. Results: Fifteen AGVA and nine control patients died. In each group seven deaths were noncardiac. Six nonsudden and two sudden cardiac deaths (SCD) occurred in the AGVA group at 2‐36 months after CABG and two nonsudden cardiac deaths in the control group at 3 and 35 months after CABG (p = 0.053). Both SCDs occurred 33 months after CABG after new events known to predispose to SCD. In 18 of 30 patients AGVÀ was no longer present when ambulatory ECG monitoring was repeated 36 ± 11 months after CABG. Conclusions: AGVA after CABG was not a marker of an early sudden cardiac death. In 60% of patients not treated with antiarrhythmic drugs, AGVA was no longer present late after operation.
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