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Biomedical subjects

M D Klein

Publications and source records attributed to M D Klein.

At least 127 records · Page 7Linked to original sources
PubMed1980

Antiarrhythmic efficacy, pharmacokinetics and clinical safety of tocainide in convalescent myocardial infarction patients.

The antiarrhythmic efficacy and pharmacokinetics of tocainide, an oral analog of lidocaine, was evaluated in 18 hospitalized convalescing myocardial infarction patients. Holter ECG tapes were recorded daily during two-day placebo therapy preceding and succeeding two days of tocainide treatment. Left ventricular function was characterized from prior or subsequent arteriographic studies (ten cases) or from radionuclide scanning (eight cases). Tocainide dosage was 17.7 +/- 4.9 SD mg/kg/day. Plasma half-time of elimination was 19.1 +/- 6.8 hours (r = 0.9). Tocainide had no significant effect on heart rate, pulse rate, or QTC intervals and did not worsen chronic heart failure, even in patients with ejection fraction < 30%. In seven of 18 patients, tocainide significantly reduced ventricular premature beat (VPB) frequency as compared to predrug and postdrug placebo periods. Drug responders averaged a 200 to 545% reduction in VPB frequency at tocainide blood levels of > 3.5 microgram/ml.

Adult↗
PubMed1980

Incomplete rotation of the intestine with a normal cecal position.

Nineteen patients with incomplete rotation of the intestine, seen during a 3-year period, are presented. Six patients (32%) had a normal cecal position but an abnormal duodenojejunal junction. Three of these patients had a midgut volvulus, and one had obstructing duodenal bands. The two remaining patients were premature and had postnatal fixation of the duodenojejunal junction over a 10-month to 2-year period.

Cecum↗
PubMed1979

Left ventricular false aneurysm after coronary bypass surgery: radionuclide diagnosis and surgical resection.

A patient with left ventricular pseudoaneurysm formation resulting from myocardial infarction 4 years after coronary bypass surgery is described. The pseudoaneurysm was diagnosed with gated cardiac blood pool imaging and was subsequently successfully surgically repaired. Postoperative pericardial abnormalities predisposing to the possible development of a false aneurysm are discussed. Also, clinical situations in which pseudoaneurysm should be suspected are described, and appropriate diagnostic approaches are outlined.

Coronary Artery Bypass↗
PubMed1978

ST segment changes post-infarction: predictive value for multivessel coronary disease and left ventricular aneurysm.

To ascertain whether exercise testing might predict multivessel coronary disease and left ventricular aneurysm after a myocardial infarction, 154 patients with a single documented myocardial infarction who had both exercise testing and coronary angiography were grouped according to whether they had greater than or equal to 1 mm ST depression, greater than or equal to 1 mm ST elevation, or neither during exercise testing: 83 patients developed ST depression alone (group 1); 22 patients had ST elevation with concomitant ST depression in other leads (group 2); 19 patients had ST elevation alone (group 3); and 30 patients had no ST changes (group 4). Multivessel disease, defined as greater than or equal to 70% luminal narrowing in two or more coronary vessels, was present in 76% (63 of 83) of group 1, 91% (20 of 22) of group 2, 21% (four of 19) of group 3, and 13% (four of 30) of group 4. A left ventricular aneurysm was present in 31% (26 of 83) of group 1, 68% (15 of 22) of group 2, 79% (15 of 19) of group 3, and 40% (12 to 30) of group 1. We conclude that ST changes during exercise testing in patients after a myocardial infarction can reliably predict the extent of coronary disease and the presence of a left ventricular aneurysm; ST depression with or without ST elevation predicts multivessel disease; ST elevation alone or a negative exercise test suggests single vessel involvement; and ST elevation with or without ST depression predicts left ventricular aneurysm.

Adult↗
PubMed1978

Trifascicular and complete heart block with anterior myocardial infarction. Electrocardiographic patterns and long-term medical management.

A 45-year-old man exhibited various patterns of delay in trifascicular conduction, culminating in complete heart block during acute myocardial infarction. A temporary pacemaker was utilized for the short period of heart block. Delay in ventricular conduction subsided, and the patient refused implantation of a permanent pacemaker. Ventricular irritability, which was detected eight months later, was suppressed with administration of digitalis, guided by testing with acetylstrophanthidin. Neither heart block nor delay in ventricular conduction recurred during 43 months after the infarction. In certain patients with heart block complicating anterior myocardial infarction, long-term prognosis may be dictated by coronary and myocardial residual function, rather than by the hazard of recurrent heart block.

Bundle-Branch Block↗
PubMed1976

The practice of surgery in the fourteenth century.

Henri de Mondeville details a method of wound healing that emphasizes early debridement and primary closure. In Guy de Chauliac's advice on the treatment of groin hernias, he demonstrates an early if unsophisticated understanding of the principles of high ligation of the sac and repair of the direct defect.

Europe↗
PubMed1976

Vectorial characteristics of ventricular extrasystoles stimulated during cardiac catheterization.

Ventricular extrasystoles (VES) from different areas of the ventricular muscle mass were obtained by mechanical stimulation of inflow and outflow regions of the right ventricle (RV) and apical and basal portions of the left ventricle (LV) during cardiac catheterization. Cube system vectorcardiogram (VCG) patterns of VES from each location were analyzed to determine the specificity of vector orientation from each site. Transverse plane VCG distinguished between nonseptal LVES and RVES, while a combination of transverse and either sagittal or frontal planes permitted further localization of septal VES to inflow or outflow regions of the RV and apical and basal areas of the LV.

Adult↗
PubMed1976

Effects of isometric exercise on the end-diastolic pressure, volumes, and function of the left ventricle in man.

Changes induced in left ventricular (LV) hemodynamics by isometric exercise were analyzed in 43 patients: 30 with coronary heart disease (CAD), four with noncoronary heart disease, nine normal. Volumes were angiographically determined and correlated with left ventricular end-diastolic pressure (LVEDP) both at rest and during the fifth minute of 30% sustained handgrip (HNG). All normals and eight with CAD improved LV function during HNG. LVEDP decreased or remained constant, end-diastolic volume (EDV) decreased, end-systolic volume (ESV) decreased, as ejection fraction (EF) remained constant. None of these eight CAD cases altered their regional LV contraction pattern during HNG. Twenty-five patients, 21 CAD and four nonCAD, showed diminished LV function during HNG. LVEDP increased, EDV decreased, ESV increased, as EF declined. In these 21 CAD patients, at least one major coronary vessel was narrowed 70% or more and, with but two exceptions, was not supported by adequate collaterals. In 18, new asynergic zones developed in previously normally contracting areas or pre-existing asynergic zones extended during HNG.

Cardiac Output↗
PubMed1976

Mechanisms of arrhythmias in chronic obstructive lung disease.

Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.

Aged↗
PubMed1975

Atropine dose in acute myocardial infarction in man.

Heart rate response to intravenous atropine therapy in acute myocardial infarction (MI) was assessed from detailed studies performed on 18 of 492 consecutively admitted coronary care unit patients. Atropine was given for extreme bradycardia (less than 40/min) or bradycardia (less than 60/min) coincident with hypotension or ventricular premature beats. 14 patients had posterior and 4 anterior infarction. Degree of cardioacceleration evoked by atropine depended upon drug dose and route of administration. Atropine, 0.0053-0.0088 mg/kg, given within 15 sec increased heart rate by 20-72/min but never beyond a peak rate of 120. Larger atropine doses, 0.120-0.148 mg/kg, increased heart rate by 51-92/min and, in four to five instances to a peak rate exceeding 120/min. Intramuscular atropine was associated with paradoxical slowing of heart rate in one case. Multiple neural, hormonal, and circulatory factors can modify heart rate response to fixed amounts of intravenous atropine but 0.008 mg/kg represents a safe and suitable initial drug dose for use in acute MI.

Acute Disease↗
PubMed1974

Hemoglobin affinity for oxygen in the anginal syndrome with normal coronary arteriograms.

Oxyhemoglobin dissociation (OHD) curves were performed on whole blood (WB) from 20 patients with anginal pain, normal hemodynamics, and normal coronary arteries, as demonstrated by selective coronary cinearteriography. OHD curves in 19 of 20 patients, from zero to full saturation, were nearly identical to those in normal control subjects with values for P(50) (Po(2) at 50% saturation and pH 7.4) of 26.7+/-1.5 (mean+/-SD of the mean) torr (mm Hg) and red blood cell (RBC) levels of 2,3-diphosphoglyceric acid (2, 3-DPG) of 0.72+/-0.10 (mean+/-SD of the mean) M/M hemoglobin (Hb). Normal values for nonsmoking adults were: P(50), 26.6+/-1.4 (mean+/-SD of the mean) torr: and RBC 2,3-DPG, 0.81+/-0.09 (mean+/-SD of the mean) M/M Hb. Mean levels of carbon monoxide were normal at 0.14+/-0.01 (mean+/-SEM) ml/100 ml WB in 10 patients who were nonsmokers and 0.45+/-0.15 (mean+/-SEM) ml/100 ml WB in 10 smokers. In one patient, a heavy smoker with markedly elevated blood carbon monoxide levels, an abnormal leftward shift of the OHD curve was observed. This was corrected after discontinuation of smoking. In utilizing these methods, we could not detect consistent abnormalities of Hb affinity for oxygen at rest in the patients studied, which suggests that a defect in oxygen transport at rest is an unlikely explanation for the symptoms of chest pain in patients with the anginal syndrome and normal coronary arteriograms.

Adult↗