Percutaneous pulsed laser-assisted balloon angioplasty guided by spectroscopy.

Percutaneous laser angioplasty was performed in 19 patients with total superficial femoral calcified and noncalcified (4 to 25 cm length) occlusions; a pulsed dye laser of 480 nm was used with a pulse duration of 2 musec/pulse. The treatment laser was guided by a 325 nm diagnostic laser that induced fluorescence. The laser system operated through a single 200 or 500 microns optical fiber. Computerized spectral analysis of the tissue fluorescence located at the distal of the fiber tip allowed the treatment laser to be emitted on the atheroma and not on the arterial wall. Uniform success in primary laser recanalization was demonstrated, which allowed for subsequent balloon dilatation in all but one patient. One mechanical fiber perforation, two mechanical fiber dissections, one guidewire perforation, and one guidewire dissection occurred, but no complications resulting from the treatment or diagnostic laser were observed. The safety of the procedure appears to be enhanced by the spectroscopic guidance system, which allows recognition of plaque. The pulsed dye treatment laser was well tolerated and effective even in heavily calcified arteries.

Methionine intolerance: a possible risk factor for coronary artery disease.

Homocystinuria, an inherited disorder associated with premature atherosclerosis, represents a severe form of methionine intolerance. To analyze the importance of milder forms of methionine intolerance in the genesis of vascular disease, the relation between provokable methionine intolerance and coronary artery disease was investigated. In a group of 138 men, aged 31 to 65 years (mean 53), referred for cardiac catheterization, plasma homocystine was measured before and 6 hours after an oral l-methionine load (0.1 g/kg). Thirty-nine subjects found to have normal coronary arteries had a mean post-load plasma homocystine level of 0.59 +/- 0.37 mumol/liter. A criterion at the 95th percentile (1.64 SD above the mean) was selected and applied to the remaining 99 subjects with coronary artery disease (0.70 +/- 0.68 mumol/liter). Sixteen (16%) of 99 subjects with coronary artery disease exceeded this level as compared with 1 (2%) of 39 subjects without coronary artery disease (p less than 0.04). The risk of coronary artery disease in men with provokable methionine intolerance was increased sevenfold as estimated by the odds ratio. By correlation matrix and multivariate regression analyses, provokable homocystinemia was predictive of coronary artery disease and was independent of tobacco smoking, hypertension, diabetes mellitus, serum cholesterol and age. It is proposed that men with mild methionine intolerance exposed to the high methionine content of the Western diet may develop intermittent homocystinemia and thus may be at greater risk for the development of coronary artery disease.

Potentiation by nifedipine and diltiazem of the hypotensive response after contrast angiography.

Arterial hypotension has been demonstrated after left ventriculography using currently available ionic contrast agents. This adverse hemodynamic response is significantly decreased with the newer nonionic contrast agents. Calcium channel antagonists also produce a hypotensive response. The potentially accentuated hypotensive response after bolus contrast angiography in patients receiving the calcium antagonists nifedipine and diltiazem was evaluated. Three contrast agents were compared: two ionic agents (Renografin-76 and Hypaque-76) and a nonionic agent (iopamidol). The hemodynamic response after left ventriculography was assessed in 125 patients, 65 receiving nifedipine or diltiazem and 60 not receiving these drugs. Baseline clinical characteristics were similar in all patient groups. The hypotensive response was significantly greater after left ventriculography with the ionic agents than with the nonionic agent. In those patients receiving nifedipine or diltiazem, the hypotensive response after bolus contrast angiography using the ionic agents occurred earlier after contrast injection (4.2 +/- 3.1 versus 12.9 +/- 6.0 seconds, p less than 0.0001), was more profound (maximal decrease in systolic arterial pressure, 48.5 +/- 13.9 versus 36.9 +/- 13.1 mm Hg, p less than 0.001) and was more prolonged (62.3 +/- 11.0 versus 36.4 +/- 12.0 seconds, p less than 0.0001) than in patients not receiving these drugs. A comparison of the two ionic contrast agents showed no significant difference in the hypotensive response. There was no difference in the hemodynamic response after angiography among patients receiving iopamidol alone and those receiving iopamidol and calcium antagonists. Thus, patients receiving the calcium antagonists diltiazem and nifedipine and undergoing left ventriculography with ionic contrast agents are at added risk for accentuation and prolongation of the hypotensive response.

Alterations in left ventricular function, coronary hemodynamics and myocardial catecholamine balance with MDL 17043, a new inotropic vasodilator agent, in patients with severe heart failure.

To evaluate changes in myocardial energetics and systemic and cardiac sympathetic activity associated with improved left ventricular function after MDL 17043, a new inotropic vasodilator agent, systemic and coronary hemodynamics and myocardial catecholamine balance were determined in 17 patients with severe heart failure. After the administration of MDL 17043, cardiac index increased by 67% and pulmonary capillary wedge pressure decreased (25 +/- 5 to 14 +/- 7 mm Hg, p less than 0.01), indicating improved left ventricular function. Coronary sinus blood flow (75 +/- 29 to 111 +/- 51 ml/min, p less than 0.01) and myocardial oxygen consumption (9.9 +/- 3.3 to 11.8 +/- 5.4 ml/min, p less than 0.05) increased despite decreased myocardial oxygen extraction (11.7 +/- 2 to 10.1 +/- 3.3 vol%, p less than 0.05) and a higher coronary sinus oxygen content. Although transmyocardial lactate extraction remained unchanged, increased myocardial oxygen consumption has potential deleterious effects on myocardial metabolic function. Arterial norepinephrine concentrations and transmyocardial norepinephrine release also remained unchanged. These findings suggest that MDL 17043 improves left ventricular pump function, but produces no detectable change in systemic and cardiac sympathetic activity. Improved left ventricular function is associated with increased myocardial oxygen consumption despite primary coronary vasodilation.

Hyperkalemia complicating digoxin toxicity in a patient with renal failure.

We describe the occurrence of hyperkalemia in a stable hemodialysis patient who developed digoxin toxicity. The patient had been receiving digoxin for 2 years. His maintenance digoxin dose was increased from 0.125 to 0.25 mg three times a week, which resulted in a toxic serum level of 4.9 ng/mL (therapeutic range is 0.8 to 2.0 ng/mL). As a consequence of the digoxin toxicity, he became hyperkalemic (7.8 mEq/L), and this value returned to normal only after the digoxin level was lowered by a combination of oral charcoal and dialysis. This study shows how readily hyperkalemia can occur in an anephric patient manifesting digoxin toxicity. Thus, potentially lethal hyperkalemia can occur in hemodialysis patients who ingest therapeutic quantities of digoxin. Digoxin toxicity should be added to the differential diagnosis of hyperkalemia in patients with renal failure. This can occur despite the absence of a history of massive ingestion of a cardiac glycoside.