Percutaneous coronary laser balloon angioplasty: initial results of a multicenter experience.

A multicenter clinical trial was initiated to test the potential safety and short-term efficacy of a percutaneous coronary application of laser balloon angioplasty, which has been shown experimentally to alleviate the common causes (dissection, recoil, thrombus) of suboptimal luminal results of conventional balloon angioplasty. Fifty-five patients, the majority (62%) of whom had relatively high risk lesions, were treated in 10 centers with a laser balloon that was identical in size (3 x 20 mm) to a balloon used for conventional balloon angioplasty performed on the same lesion immediately before laser balloon angioplasty. One or more neodymium:yttrium aluminum garnet (Nd:YAG) (1,060 nm) laser doses of 250 to 450 J were each delivered over a 20 s duration per exposure. Immediately and 1 day after laser balloon angioplasty no significant adverse effects on the arterial lumen were noted in any patient. By computerized image analysis of cineangiograms initial conventional balloon angioplasty failed to achieve a minimal luminal diameter greater than 1.5 mm in 14 patients (25%), including 3 patients with acute closure. However, after subsequent laser balloon angioplasty, minimal luminal diameter exceeded this value in all patients including this subgroup. Overall, minimal luminal diameter increased from 1.74 +/- 0.46 mm after conventional balloon angioplasty to 2.32 +/- 0.31 mm after laser balloon angioplasty (p less than 0.001) with no change found on 1 day and 1 month follow-up angiograms. Thus, laser balloon angioplasty is a safe, effective procedure for improving luminal dimensions after conventional balloon angioplasty.

Carcinoma of uterine cervix with myocardial metastases associated with chest pain and asystolic arrest.

We report a case of secondary deposition of carcinoma of the uterine cervix in the myocardium with development of ischaemic cardiac pain, ST segment elevation and asystolic cardiac arrest. The coronary arteries were free of obstruction. To the best of our knowledge, this is a unique presentation of a rare myocardial metastasis.

Rat myocardial protein degradation.

1. Myocardial protein degradation rates were determined by following tyrosine release from rat isolated left hemi-atria in vitro. 2. After two 20 min preincubations the rate of tyrosine release from hemi-atria was constant for 4 h. 3. Skeletal muscle protein degradation was determined by following tyrosine release from rat isolated hemi-diaphragm (Fulks, Li & Goldberg, 1975). 4. Insulin (10(-7) M) inhibited tyrosine release from hemi-atria and hemi-diaphragm to a similar extent. A 48 h fast increased tyrosine release rate from hemi-diaphragm and decreased tyrosine release rate from hemi-atria. Hemi-diaphragm tyrosine release was inhibited by 15 mmol/l D-glucose but a variety of concentrations of D-glucose (0, 5, 15 mmol/l) had no effect on tyrosine release from hemi-atria. Five times the normal plasma levels of the branched-chain amino acids leucine, isoleucine and valine had no effect on tyrosine release from either hemi-atria or hemi-diaphragm.

Suppression of myocardial protein degradation in the rat during fasting. Effects of insulin, glucose, and leucine.

To study the effects of leucine, glucose, and insulin on myocardial protein degradation in fed and fasted nutritional states, we developed and validated a sensitive method for measuring rates of total protein degradation in rat isolated left atrial preparations. Fasting resulted in a progressive decrease in myocardial protein breakdown to 71% of control over a 24-hour period, with no further reduction in degradation rate between 24 and 72 hours of fasting. Insulin (100 mU/ml) suppressed atrial protein degradation by 38% in fed animals (P less than 0.001) and by 51% in fasted animals (P less than 0.001). Glucose alone had no effect on protein degradation in either nutritional state. At 5 times normal plasma levels, leucine suppressed protein breakdown by 21% in fed and by 15% in fasted animals. The decrease in degradation induced by fasting and the absence of an effect of glucose are in contrast to the behavior reported for skeletal muscle.

Insulin effects on monovalent cation transport and Na-K-ATPase activity.

The effects of insulin on monovalent cation transport and on Na-K-ATPase activity from intact cells, tissue homogenates, and purified enzyme of the avian salt gland were studied. Monovalent cation active transport, measured by ouabain-inhibitable 86Rb+ uptake, was significantly increased (21.9 +/- 7.3% SE) in tissue slices exposed to insulin (100 mU/ml) for 15 min. A small but significant (12.2 +/- 1.9%) increase in Na-K-ATPase activity was similarly observed after salt gland tissue slices were exposed to insulin. This increase in enzymatic activity did not occur when broken-cell homogenates were exposed to insulin. Purified preparations of Na-K-ATPase showed no insulin enhancement of activity either in the presence of optimal or less than fully activating Na+ and ATP concentrations. Na-K-ATPase activity was the same in detergent-activated homogenates of both control and insulin-treated slices, consistent with insulin activation of existing enzyme sites. These data support the hypothesis that at least part of the increase in monovalent cation active transport produced by insulin is related to enhanced Na-K-ATPase activity and indicate that the latter phenomenon is dependent on some components or properties of the intact cell.

Increase in myocardial digoxin content associated with circulatory volume overload in the dog.

1. Tritiated (12alpha-3H) digoxin (0-05 mg/kg body weight) was administered intravenously to conscious dogs with circulatory volume overload induced by previous creation of aorto-caval fistulae. Dogs were killed after 5 min, 1, or 4 h, and the myocardium sampled. Digoxin was extracted and counted and results compared to those in normal dogs. 2. At each time, myocardial digoxin concentration of all cardiac chambers in test dogs was greater than normal. Plasma digoxin concentration measured 5 min after administration was greater in dogs with fistulae but the subsequent levels were not different. 3. Anaesthetized and open-chest dogs with fistulae studied 5 min after digoxin administration had greater myocardial concentrations than similarly studied normal dogs. Although myocardial concentrations of digoxin were higher in anaesthetized than in conscious dogs the group with fistulae had higher values than did the normal group, as was the case for unanaesthetized dogs. 4. The basis for the effect of fistula is probably multifactorial. Diminised peripheral blood flow and peripheral digoxin delivery and uptake, resulting initially in higher digoxin levels in plasma perfusing the myocardium, may play a role. Increased myocardial mechanical and metabolic activity almost certainly are important. Cardiac hypertrophy, cardiac failure per se and plasma electrolyte changes are probably not. 5. The results are consistent with previously demonstrated reduced digitalis tolerance in the dog with circulatory volume overload.

Sodium- and potassium-activated adenosine triphosphatase of the nasal salt gland of the duck (Anas platyrhynchos). Purification, characterization, and NH2-terminal amino acid sequence of the phosphorylating polypeptide.

Sodium- and potassium-activated adenosine triphosphatase (NaK-ATPase) was purified from nasal salt glands of the duck (Anas platyrhynchos). Enzyme of specific activity 2,000 to 2,300 mumol of Pi/mg/hour was routinely obtained by sodium dodecyl sulfate treatment of a microsomal fraction of gland homogenate in the presence of 3 mM ATP followed by pelleting of the enzyme through a sucrose density gradient. Purified NaK-ATPase was stable for over 3 months at -20 degree. By sodium dodecyl sulfate-polyacrylamide gel electrophoresis and gel filtration chromatography purified NaK-ATPase was shown to contain two polypeptide chains of molecular weight 94,000 and 60,000, the smaller of which was a glycoprotein. Purified enzyme of activity 2,300 mumol of Pi/mg/hour bound 3,600 pmol of ouabain/mg of enzyme protein. Reaction with [gamma-32P]ATP in the presence of Mg2+ and Na+ gave 7,025 pmol of acyl phosphate/mg of enzyme protein. The turnover number calculated from phosphorylation data was 5,460 min-1. Amino acid analysis of the polypeptide components of duck salt gland enzyme after separation by gel filtration chromatography in sodium dodecyl sulfate demonstrated strong compositional homology with highly purified NaK-ATPase preparations from other organs and species. The NH2-terminal amino acid of the 94,000-dalton component was glycine and of the 60,000-dalton component, alanine. With a combination of manual sequencing and automated Edman degradation, the NH2-terminal amino acid sequence of the 94,00-dalton catalytic subunit was found to be Gly-Arg-Asn-Lys-Tyr-Glu-Thr-Thr-Ala-()-Ser-Glu.

Familial hypertrophic cariomyopathy and lentiginosis.

Members of three generations of a family studied, manifest profuse lentiginosis and hypertrophic cardiomyopathy. The autosomal dominant inheritance of this syndrome is established. Lentiginosis should alert the physician to possible underlying heart disease.

Digitalis-induced increase in aortic regurgitation and the contrasting effect of glucagon in the sedated dog.

The hemodynamic and phasic ascending aortic flow changes induced by acetylstrophanthidin and glucagon were studied in closed-chest sedated dogs with aortic regurgitation. While the positive inotropic effect of both agents was reflected in an increase in peak rate of rise of left ventricular pressure, acetylstrophanthidin increased aortic regurgitation, while glucagon decreased it. With the former, left ventricular end-diastolic pressure rose from 20+/-6 to 27+/-6 mm Hg (P < 0.005), but fell from 18+/-4 to 11+/-3 mm Hg (P < 0.001) with glucagon. Acetylstrophanthidin increased systemic vascular resistance, aortic diastolic pressure, and diastolic regurgitant flow rate, and, heart rate and the duration of regurgitation per beat and per minute being unchanged, regurgitant flow per beat increased 32+/-15% (P < 0.001). Glucagon decreased regurgitant flow per beat 27+/-14% (P < 0.001) because of abbreviation of diastole associated with tachycardia, and because of reduction in regurgitant flow rate. Despite tachycardia, the duration of regurgitation per minute was unchanged, and the small fall in regurgitant blood flow per minute was not significant, but this pertained in the face of 47% increase in effective cardiac output (P < 0.001). In contrast, acetylstrophanthidin increased regurgitant flow per minute 28+/-14% (P < 0.001) without change in effective cardiac output. The increase in cardiac contractility, tachycardia, and systemic vasodilatation induced by glucagon preferentially enhanced forward blood flow, which led to reduction in left ventricular volume overload, while it increased cardiac output. Contrarily, acetylstrophanthidin increased aortic regurgitation and, despite its inotropic effect, increased left ventricular volume overload without an increase in cardiac output.