Carl S. Alexander

Cobalt and the Heart

Excerpt In late 1963 or early 1964 certain brewers in Quebec, Canada, and the United States began adding cobalt to beer in order to stabilize the foam. Within months an epidemic form of fulminating...

Lowering of ethanol-derived circulating blood acetaldehyde in rats by D-penicillamine

Abstract The sulfhydryl amino acid, D-penicillamine, but not L-cysteine or L-cystine, when administered to disulfiram-treated rats 1 hour before a dose of ethanol lowered the ethanol-derived, circulating blood acetaldehyde to 10% of control values. This was accompanied by a concomitant lowering of AcH in the expired air of penicillamine-treated rats. Since blood ethanol levels were the same in saline injected controls and in sulfhydryl amino acid-treated rats, this lowering of blood acetaldehyde was not due to any malabsorption of ethanol or to inhibition of the enzyme(s) that metabolize ethanol. By administration of D-penicillamine in multiple, divided doses, blood acetaldehyde generated during ethanol metabolism was reduced an average of 70% over an 8 hour period.

Bradycardia with Mitral Valve Prolapse: A Potential Mechanism of Sudden Death

Eleven members of a family with a high prevalence of mitral valve prolapse were investigated. Seven had documented sinus bradycardia, and five had mitral valve prolapse. Three patients with both mitral valve prolapse and bradycardia had recurrent syncope reproduced by simple head-up tilting, and in one patient this resulted in asystole. The hemodynamic response to isoproterenol and phenylephrine administration were normal. Supine plasma norepinephrine levels were normal in all three and increased appropriately in two of three patients after tilting. Atrial pacing studies documented marked prolongation of atrial-His intervals and inability to maintain 1:1 atrioventricular conduction when paced at a rate of 120/min. These findings were reversed by atropine. This family shows a close correlation between mitral valve prolapse and potentially lethal bradycardia. Excessive vagal tone is believed to be responsible for both bradycardia and sinus arrest, which in two patients was prevented by permanent demand pacing.

Diagnosis of idiopathic hypertrophic subaortic stenosis by right ventricular septal biopsy

Abstract The clinical, hemodynamic and histologic features of six adult male patients with idiopathic hypertrophic subaortic stenosis are compared with those of three adult patients with aortic valve stenosis. All nine patients had a right ventricular septal biopsy, and the tissue so obtained was examined by light and electron microscopy. The characteristic disorganized architecture with random orientation of myoflbers seen by others in tissue removed from the left ventricular outflow tract was also observed in each specimen from patients with idiopathic hypertrophic subaortic stenosis but in none of those from patients with aortic stenosis. The changes were even more striking and bizarre when viewed under the electron microscope. Whorled collagen fibers in the tissue of three patients with Idiopathic hypertrophic subaortic stenosis resembled the whorled myofibers. Neither structural abnormality was seen in tissue obtained from patients with aortic stenosis. Thus, biopsy of the right ventricular septum can differentiate idiopathic hypertrophic subaortic stenosis from aortic stenosis, even when the specimens are examined by light microscopy alone.

Traumatic tricuspid insufficiency

Abstract In a 45 year old farmer, free tricuspid insufficiency developed after blunt injury to the right anterior lower chest by a heavy flying object. The clinicle course was complicated by recurrent atrial flutter with 2:1 atrioventricular block and right to left shunt through a patent foramen ovale. Diagnosis was based on clinical, roentgenologic and catheterization data and was confirmed by surgical findings. Tricuspid insufficiency was caused by thin atrophic retracted tricuspid leaflets which were attached normally to the annulus and intact papillary muscles. However, the attached chordae were unusually elongated. Six months after replacement of the tricuspid valve, the heart size returned to normal and the patient was again performing heavy farm labor.

Hemolytic Anemia Due to Progressive Enlargement of Silastic Ball Component of Aortic Prosthesis

The patient described developed hemolytic anemia following insertion of a Starr-Edwards aortic valve prosthesis. No diastolic murmur was heard and no insufficiency was detected. The hemolytic anemia was progressively more severe and uncompensated despite various medical measures.The anemia was characterized by fragmented erythrocytes in the peripheral blood, reticulocytosis, elevation of plasma heme pigments augmented by exercise, increased fecal urobilinogen, and iron loss in the urine. Studies of chromium-51-tagged erythrocytes indicated an extracorpuscular mechanism of hemolysis.At reoperation the ball component of the prosthesis was found to be enlarged and obstructing blood flow. Chemical analysis of the ball showed significant cholesterol and lipid deposits. The hemolysis disappeared after the prosthesis was replaced with a homograft valve. Ferrokinetic studies showed rapid plasma clearance and incorporation into circulating erythrocytes. Triglycerides were elevated during the period of hemolysis. Red cell membrane lipids were normal.

Metabolism of puromycin aminonucleoside in the normal, "pre-nephrotic," and nephrotic rat.

Summary Approximately 80% of injected aminonucleoside-8-C14 is excreted in the urine and feces within 24 hrs by the rat. The principal urinary products are unchanged amino-nucleoside, the monodemethylated analog, and allantoin. Daily administration of aminonu-cleoside for 12 days did not influence the course of its own metabolism.

Alcohol and the Heart

Excerpt Earlier in this century much of clinical medicine in large urban hospitals was concerned with the diagnosis and management of syphilis and tuberculosis. Today, heart disease, cancer, and th...

Acetaldehyde Metabolism by the Rat Heart

Summary Isolated beating rat hearts perfused with [1,2-14C] acetaldehyde oxidize the compound to 14CO2. Inhibition of the oxidation by pretreatment in vivo with disulfiram suggests the involvement of a myocardial aldehyde dehydrogenase. The dehydrogenation of acetaldehyde may be rate-limiting since acetate oxidation to carbon dioxide proceeds faster than acetaldehyde oxidation in the perfused rat heart. We are grateful to Steve Altman for helpful discussion and technical assistance.

Abnormal amino acid and lipid composition of aortic valve in relapsing polychondritis.

Abstract A 30 year old man had the clinical findings of relapsing polychondritis including pain in the lower back, saddle nose deformity, nerve deafness, joint swelling and, finally, intractable heart failure due to mitral and aortic regurgitation. Both valves were replaced by prostheses, and the patient returned to his job 6 months later. Results of histologic examination of the ascending aorta and valves were compatible with relapsing polychondritis and showed destruction of collagen, elastic tissue and cystic changes indistinguishable from cystic medial necrosis of the aorta. Amino acid and lipid composition of the aortic valve showed striking abnormalities compared to findings in valves of 4 normal human hearts.