Cardiac catheterization through the internal jugular vein in pediatric patients. An alternative to the usual femoral vein access.

The percutaneous femoral vein approach is used routinely for cardiac catheterization in the pediatric age but in some children, it may be impossible as in the case of iliac vein or inferior vena cava thrombosis due to previous cardiac catheterization, or inconvenient as for right ventricular endomyocardial biopsies. In the period between 1982 and 1990, 160 cardiac catheterizations or right ventricular endomyocardial biopsies were performed in 102 children. Patients ranged in age between 2 months and 17 years (mean, 3.8 years) and in weight from 3.2 to 57.3 kg (mean, 14.4 kg). Indications for the internal jugular vein approach were as follows: (1) thrombosis of the inferior vena cava due to previous cardiac catheterization in 42 patients (41 percent); (2) right ventricular endomyocardial biopsy after cardiac transplant in 19 patients (19 percent); (3) control catheterization of the pulmonary arteries following classic or bidirectional cavopulmonary anastomosis in 16 patients (16 percent); (4) superior vena cava obstruction following Mustard's procedure in 14 patients (14 percent); (5) failed percutaneous femoral venous approach in six patients (6 percent); and (6) absence of the hepatic segment of the inferior vena cava in four patients (4 percent). The right or left internal jugular vein could be entered in all but three procedures (98 percent). Seventeen patients had more than one procedure through the same internal jugular vein and the vein was found patent in all. A complete right heart cardiac catheterization was performed using this route. Right ventricular endomyocardial biopsy and interventional procedure were performed through this route. Two major complications occurred. A patient developed a central transient ischemic attack and another patient developed a persistent Horner syndrome. Accidental carotid puncture occurred in five patients without consequences. Our data indicate that cardiac catheterization in infants and children can be performed safely through the internal jugular vein, with a high success rate and a low incidence of major complications.

Apparent failure of edetic acid chelation therapy for the treatment of coronary atherosclerosis.

Patients diagnosed with incurable or fatal diseases may seek alternatives to standard medical therapy and spend significant amounts of money for these therapies. One alternative medical therapy, chelation therapy with edetic acid (EDTA), has gained considerable popularity for the alleged treatment of atherosclerotic vascular disease; however, its efficacy for this indication remains unproven and its use is controversial. We present a case in which chelation therapy was unsuccessful in treating coronary atherosclerosis and review reports that substantiate a lack of efficacy using chelation therapy in the treatment of coronary atherosclerosis. Treatment of atherosclerotic-related diseases using chelation therapy should be discouraged by health professionals. Patients should be counseled regarding the risk of improper diagnosis and treatment of their disease.

[Relation of the patterns of syndrome differentiation and features of coronary and left ventricular angiocardiography in coronary heart disease].

From 1986-1988, 43 CHD patients were analyzed on the relationship between the patterns of syndrome differentiation and the features of coronary and left ventricular angiocardiography. There were 17/18 cases (94.41%) with fixed stenotic lesions of coronary arteries in the pattern of blood stasis; 1/18 cases (5.5%) had coronary spasm; none was normal. The cases with blood stasis pattern were mostly of old myocardial infarction, effort angina and effort coexisting with spontaneous angina. They complained a fixed squeezing substernal pain provoked by physical exertion. In 14/25 cases (56%) of syndrome differentiation with Qi deficiency and Qi stagnation, the coronary arteries were normal. 3/25 cases (12%) had coronary arterial spasm and 8/25 cases (32%) had stenotic lesions in coronary artery. The cases of Qi deficiency and Qi stagnation were mostly of spontaneous and atypical angina. They complained precordial distress or pain with undefinite location associated with shortness of breath and fatigue. The distress was relieved by a deep breath. Abnormal ejection fraction was seen mostly in the pattern of Qi symptoms and signs but less in the pattern of blood stasis (P less than 0.002). There was no significant difference in platelet aggregation test and echocardiogram between the two patterns.

Gallbladder opacification in infants following high dose angiocardiography.

Seven infants in congestive heart failure underwent high dose angiocardiography for diagnosis of severe congenital heart disease and subsequently displayed delayed opacification of the gallbladder. Biliary excretion of sufficient volume to opacify the gallbladder occurred despite structurally normal kidneys and no evidence of renal failure. Decreased renal clearance of contrast due to generalized diminution of glomerular filtration is postulated. The high doses of contrast and slow renal clearance allowed a relatively increased rate of hepatobiliary excretion and subsequent observation of the opacified gallbladder on abdominal radiographs. This phenomenon may not be as uncommon as is generally thought but its timing and location often do not allow an opportunity to make this observation.

Exact mechanisms contributing to instability and refractoriness to therapy in patients with unstable angina: coronary arteriographic evaluation.

Ninety one patients with unstable angina were evaluated by clinical and angiographic study. Of 91 patients, 42 (46%) responded poorly to the intensive medical treatment. Emergency coronary arteriography was then performed on these patients. The important pathoanatomical mechanisms contributing to instability of angina pectoris and/or refractoriness to the intensive medical treatment were observed in 19 of 42 patients (45%). These include: 1) More severe disease with left main lesion; 2) Refractory coronary spasm; 3) Coronary dissection; 4) Rapid progression of atherosclerosis; 5) Ulcerating plaque and 6) Coronary thrombus. Our results presented here suggest that an appropriate knowledge regarding pathophysiology might improve the approach to treatment.

Treatment of tachycardias associated with the Wolff-Parkinson-White syndrome by transvenous electrical ablation of accessory pathways.

Three patients with tachycardias associated with the Wolff-Parkinson-White syndrome had failed to respond to antiarrhythmic drugs and underwent transvenous ablation of accessory pathways. Intracardiac studies located the site of accessory pathway to the septum in two patients and mid-posterobasal left atrioventricular junction in one. Ablation was performed by positioning an electrode lead as close as possible to the accessory tract and delivering shocks of 50 to 100J using a conventional defibrillator. In all patients the accessory pathway was abolished after the first three shocks. In two patients followed for four and nine months there was no recurrence of tachycardia or pre-excitation. The other patient developed pre-excitation again three weeks later and repeat ablation was performed. This patient has been followed for six months with no evidence of a recurrence of pre-excitation. This method may provide a valuable alternative to pacemaker and surgical treatment in selected patients with drug resistant arrhythmias associated with accessory atrioventricular connexions.

Molecular markers of contrast media-induced adverse reactions.

Currently used routine laboratory screening methods are not reliable in the prediction of contrast media-related adverse reactions. Cost-effective laboratory methods for various molecular markers of pathophysiologic activation have now become available. In vitro activation tests in high-risk patients may prove to be useful in the prediction of contrast-induced activation of various adverse reactions. If prior clinical evaluation of a patient suggests an ongoing pathologic process, profiling of the following molecular markers may prove to be useful and helpful in avoiding contrast-induced adverse reactions: Fibrinopeptide A, platelet factor 4, thromboxane B2, 5-HETE, physiologic inhibitors of proteases, B beta 15-42 related peptides, bradykinin/kininogen, and anaphylactozins. In patients suspected of reacting to contrast agents, a small dose of 1 to 5 ml can be injected as a bolus and molecular marker profiling on blood drawn after the infusion may prove to be useful screening tests. Additional clinical studies are needed to prove this. However, this screening test should be performed with extreme caution, since some of the patients are known to react to as little as 1 ml dose. The safety of newly developed nonionic contrast agents can be readily assessed by profiling various molecular markers of adverse reactions, which provide a more reliable and quantitative assessment of contrast-induced adverse reactions. Based on molecular marker profiling, various prophylactic agents can be given to high-risk patients to avoid contrast-induced adverse reactions.

Congestive cardiomyopathy and the selenium content of serum.

A deficiency of selenium is suspected to be involved in the pathogenesis of congestive cardiomyopathy. Therefore the serum selenium content of 20 patients with proven congestive cardiomyopathy was measured and compared to that of a healthy control group. The serum selenium content of the patients with cardiomyopathy was found to be different from that of the healthy control group. The mean value of selenium in serum for the control group was 80.1 micrograms Se/1 (SD +/- 13.2) within a range of 53 and 117 micrograms Se/1. From the 20 patients with congestive cardiomyopathy six patients showed selenium concentrations in the normal value range of the control group; in the serum of 14 patients a distinct lower selenium content was found (mean value 47.8 micrograms Se/1 (SD +/- 16.2)) within a range of 23 and 70 micrograms Se/1. A positive correlation was found between serum selenium content and the left ventricular ejection fraction. Our results suggest that a deficiency of selenium may be present in a number of patients with congestive cardiomyopathy.

Protection of the ischemic myocardium with calcium antagonistic drugs.

Ligation of the coronary artery to produce myocardial infarction experimentally was performed in 41 mongrel dogs. The dogs were then treated with niludipine or nifedipine. Niludipine in doses of 0.05 mg/kg/day (niludipine A group) and 0.1 mg/kg/day (niludipine B group) or nifedipine 0.05 mg/kg/day (nifedipine group) was administered for 7 postoperative days. The animals were sacrificed, their hearts removed and extent of myocardial damage studied. 1. The size of infarctions measured by 99mTc-PYP myocardial scintigrams of the isolated heart was significantly smaller in the niludipine A group. 2. The degree of ischemia indicated by LDH isoenzyme patterns was lowest in the niludipine A group followed by nifedipine and niludipine B group in this order. The value for H subunits of LDH isoenzymes on the subepicardial side was higher in the nifedipine group. 3. Histopathological findings varied from specimen to specimen, but in general the niludipine A group showed best improvement. Our results suggest that the calcium antagonistic drugs, niludipine and nifedipine, seem to have myocardium protective properties in dogs. To what degree these findings can be applied clinically needs further studies.

Randomized double-blind comparison of nifedipine and isosorbide dinitrate in patients with coronary arterial spasm.

The effects of nifedinpine and isosorbide dinitrate on the frequency of angina and consumption of nitroglycerin were studied in 19 patients with coronary arterial spasm. After a lead-in phase, the patients were randomized to treatment with either nifedipine or isosorbide dinitrate. After dose titration (40 to 120 mg/day) and evaluation, they were given the alternate therapy. During the initial segment of the double-blind phase, one patient died suddenly (nifedipine phase), one dropped out of the study (nifedipine phase) and another was unable to tolerate therapy (isosorbide dinitrate phase). In the other 16 patients, the mean frequency of angina was less during therapy with both nifedipine (0.69 episode/day, p less than 0.05) and isosorbide dinitrate (0.77 episode/day, p less than 0.05) phases than during the lead-in phase (1.71 episodes/day). The mean frequency of angina was similar in the nifedipine and isosorbide dinitrate phases. A 50 percent or greater decrease in frequency of angina compared with lead-in phase values occurred in 13 of 18 patients during treatment with nifedipine and in 10 of 16 during treatment with isosorbide dinitrate. Of the 16 patients who completed both double-blind phases, 7 showed greater improvement (that is, a 50 percent or greater decrease in frequency of angina) with nifedipine than with isosorbide dinitrate); 6 others showed greater improvement with isosorbide dinitrate, and the other 3 had a less than 50 percent difference in frequency of angina with the two drugs. These findings in a limited number of patients suggest that both nifedipine and isosorbide dinitrate are effective in certain patients with coronary spasm but that neither drug is clearly superior.

Refractory variant angina controlled with combined drug therapy in a patient with a single coronary artery.

A young man with a single left coronary artery and refractory variant angina is described. Spontaneous coronary artery spasm developed during coronary arteriography at the site of a 50% fixed left anterior descending coronary artery stenosis. Frequent episodes of rest angina with transient ST segment elevation persisted in hospital in spite of treatment with three different calcium antagonist drugs. Symptoms disappeared only when the combination of nifedipine, diltiazem, isosorbide dinitrate, and nitroglycerin ointment were given. Ergonovine testing was used to objectively assess the response to treatment.

An assessment of lithium borate thermoluminescent dosimeters for the measurement of doses to patients in diagnostic radiology.

A pilot survey of doses to patients undergoing four types of radiological procedure--barium enemas, intravenous pyelography, cardiac catheterization and mammography--has been made using lithium borate TL dosimeters. The survey was designed to test the operational suitability of the dosimetry system and to gain experience and gather data for the planning of further larger surveys. The TL dosimeters were calibrated against conventional ionization chambers, and then used on patients for determining gonad doses and maximum doses to the skin. Few difficulties were encountered in using the system. The measured doses to patients have been compared with previous determinations by other authors and reasonable agreement demonstrated.

Idiopathic ventricular tachycardia. An intracardiac electrical, hemodynamic and angiographic assessment of six patients.

Six patients with idiopathic paroxysmal ventricular tachycardia were investigated by external electrocardiography, intracardiac electrography and pacing, exercise testing, cardiac catheterization and coronary angiography. All had normal hemodynamics and coronary arteries. His bundle electrography proved ventricular origin in five; one had no paroxysmal ventricular tachycardia during His bundle electrography. Treatment with diphenylhydantoin, 4.2 to 8.0 mg/kg/day, and propranolol, 0.8 to 2.7 mg/kg/day, appeared effective, well tolerated therapy in three, and procainamide and propranolol in one requiring medical treatment. Abstinence from tobacco and coffee abolished paroxysmal ventricular tachycardia in one of two who required no medication. The other has no recurrence of paroxysmal ventricular tachycardia since study.