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Biomedical subjects

K M Kessler

Publications and source records attributed to K M Kessler.

At least 145 records · Page 8Linked to original sources
PubMed1982

Handgrip exercise in normal young women: a noninvasive cardiovascular assessment.

Blood pressure, heart rate, and echocardiographic parameters of left ventricular size and shortening were measured both under baseline conditions and during handgrip exercise (50% maximum handgrip effort held to fatigue) in 20 normal women (20 through 29 years of age). As a group, there was a significant increase in heart rate (72 +/- 10 vs 83 +/- 12; P less than .001), systolic blood pressure (111 +/- 8 vs 133 +/- 14 mm Hg; P less than .001), diastolic blood pressure (67 +/- 8 vs 89 +/- 12 mm Hg; P less than .001), and calculated cardiac output (4.3 +/- 1.5 vs 5.2 +/- 1.7 liters/minute; P less than .005). There was no significant change in left ventricular internal dimension in diastole or systole, shortening fraction, or calculated stroke volume. The average group response of an increase in cardiac output secondary to an increase in heart rate is similar to that of male subjects in their second decade. Individual variability in responses was of specific interest since only three of the 20 women demonstrated a totally characteristic response to handgrip exercise. Handgrip exercise in young women may not provide a uniformly characteristic response from which to predict hemodynamic changes in a given individual and may lead to clinical misinterpretation if appropriate caution is not used.

Adult↗
PubMed1982

Simultaneous quantitation of quinidine, procainamide, and N-acetylprocainamide in serum by gas-liquid chromatography with a nitrogen-phosphorus selective detector.

We describe a single-run method for quantitating quinidine, procainamide, and N-acetylprocainamide, involving gas-liquid chromatography with a nitrogen-phosphorus selective detector. Within-run precision (CV) was 3% (x = 2 mg/L, n = 20), 6.9% (x = 4 mg/L, n = 10), and 1.5% (x = 8 mg/L, n = 8) for quinidine; 7.7% (x = 4 mg/L, n = 14), 1.6% (x = 8 mg/L, n = 16), and 2.3% (x = 12 mg/L, n = 12) for procainamide; and 6.3% (x = 5 mg/L, n = 6), 3.6% (x = 10 mg/L, n = 20), and 4.0% (x = 20 mg/L, n = 10) for N-acetylprocainamide.l Between-run precision was 3.0%(x = 2 mg/L, n = 20), 7.0% (x = 4 mg/L, n = 9), and 2.8% (x = 8 mg/L, n = 9) for quinidine; 4.7% (x = 4 mg/L, n = 10). 3.3% (x = 8 mg/L, n = 20), and 1.9% (x = 12 mg/L, n = 10) for procainamide; and 9.3% (x = 5 mg/L, n = 6), 4.3% (x = 10 mg/L, n = 20), and 3.8% (x = 20 mg/L, n = 10) for N-acetylprocainamide. Tube stoppers that contain a rubber plasticizer interfere with the technique. Clinical application and correlation with drug concentrations by this technique are discussed.

Acecainide↗
PubMed1981

Decreased quinidine plasma protein binding during hemodialysis.

Quinidine binding to serum proteins was quantitated in 10 regularly dialyzed patients with end-stage renal disease, both under baseline conditions and after heparin during a single hemodialysis. Quinidine binding was determined in vitro, after the addition of 2 micrograms/ml quinidine sulfate, by ultrafiltration combined with spectrophotofluorometry. The baseline percent unbound quinidine concentration in our patients was 6.5 +/- 2.3% (mean +/- SD), a value lower than in normal subjects (9.9 +/- 3.0%, n = 18, p less than 0.005). Binding correlated with both serum albumin (r = 0.72, p less than 0.02) and free fatty acid (r = 0.65, p less than 0.05) concentrations. After heparin there was a rise in percent unbound quinidine (12.2 +/- 5.6%, p less than 0.025) and in free fatty acid concentration (1111 +/- 1202 microEq/l, p = 0.004) in each subject. After heparin the relationship between quinidine binding and free fatty acid concentration was again evident (r = 0.97, p less than 0.001). Dynamic changes in the levels of free quinidine, as well as other drugs during hemodialysis, may require adjustments to avoid toxicity and adverse interactions.

Blood Proteins↗
PubMed1981

Age-related differences in the protein binding of quinidine.

The in vitro serum protein binding of quinidine was determined in 26 pediatric patients. Group I consisted of 6 cord blood samples obtained at the time of delivery, group II of 8 infants aged 8-18 months, and group III of 12 children over the age of 2 years. The percentage of free quinidine in group I was 39.2 +/- 10.8, group II 24.4 +/- 10.6 and group III 16.6 +/- 6.5, demonstrating a larger proportion of unbound quinidine in the newborn group and an increase in protein binding with age (p less than 0.0001). Therefore, the protein binding of quinidine is diminished in the neonate and young infant and may result in enhanced quinidine activity.

Aging↗
PubMed1981

Relationship between plasma levels of procainamide, suppression of premature ventricular complexes and prevention of recurrent ventricular tachycardia.

We compared the relationship between plasma levels of procainamide and suppression or prevention of various forms of ventricular arrhythmias in 18 patients, six of whom had premature ventricular complexes (PVCs) during acute myocardial infarction (AMI), six of whom had PVCs in the setting of stable chronic ischemic heart disease (CIHD), and six of whom had recurrent symptomatic ventricular tachycardia (VT) with chronic PVCs between episodes of VT. The mean plasma level of procainamide required for 85% suppression of PVCs in the AMI patients was 5.0 +/- 0.5 micrograms/ml, while that required for the CIHD patients was 9.3 +/- 0.7 micrograms/ml (p less than 0.05). The mean plasma level required for prevention of spontaneous episodes of symptomatic sustained tachycardia in the VT group was 9.1 +/- 3.4 micrograms/ml, while the mean level required for 85% suppression of PVCs in the same patients was 14.9 +/- 3.8 micrograms/ml (p less than 0.01). In the VT group, PVC frequency was decreased by a mean of only 36% (range 11-63%) at plasma levels of procainamide sufficient to prevent spontaneous VT. The relationship between plasma levels of procainamide and PVC suppression appears to be different in AMI and CIHD patients; furthermore, a high degree of PVC suppression is not a necessary endpoint of antiarrhythmic therapy when attempting to protect patients against recurrent symptomatic VT.

Acute Disease↗
PubMed1980

Pseudo-mitral-valve echogram following prosthetic mitral valve replacement.

Echocardiographic recordings from a patient with a prosthetic mitral valve revealed echoes within the left ventricular cavity that mimicked the motion pattern of a "normal" anterior mitral leaflet. The echo pattern was continuous, recorded from multiple views, and by two-dimensional images it was localized to the level of the papillary muscles. Although thrombus and vegetation are possibilities, this echo probably originates from a pliable chordal structure severed but not removed at the time of surgery. The apparent responsiveness to hemodynamic influences was striking, and we suggest that the prevalence and pathophysiologic implications of such findings are of potential import.

Aged↗
PubMed1980

Echocardiographic observations regarding pericardial effusions associated with cardiac disease.

Cardiac disease associated with congestive heart failure was found to be the most common cause (22 of 76) of pericardial effusion in patients referred for echocardiography. Parameters of left heart function were markedly abnormal in these patients with congestive heart failure and pericardial effusion, but were not significantly different from a group of patients with congestive heart failure without pericardial effusion. Clinical findings consistent with cardiac decompensation also failed to discern between these two groups. Nonetheless, patients with congestive heart failure with pericardial effusion had significantly larger right ventricular internal dimensions than those without effusion. Patients with pericardial effusion related to congestive heart failure (P < .01), heart disease without congestive heart failure (P < 0.001) and those patients post recent myocardial infarction (P < 0.05) had significantly larger right ventricular internal dimensions in diastole than normal subjects. Patients with pericardial effusions related to recent open heart surgery, idiopathic pericarditis or of miscellaneous causes had normal right ventricular internal dimensions. It is likely that right ventricular dilation indicates abnormal volume/pressure relationships of the right heart and that this abnormality, through alterations in venous and lymphatic drainage, underlies the accumulation of pericardial effusion in these patients with heart disease with or without congestive heart failure.

Aged↗
PubMed1980

Left ventricular size and function in women receiving oral contraceptives.

Echocardiography and systolic time-interval measurements were performed to assess left ventricular size and function in 15 women receiving oral contraceptives and in a control group. There was no significant difference in heart rate (78 +/- 9 verus 72 +/- 12 beats/min), blood pressure (116 +/- 8/72 +/- 7 versus 110 +/- 11/67 +/- 9 mmHg), left ventricular ejection time/preejection period (LVET/PEP) (0.31 +/- 0.05 versus 0.29 +/- 0.05), left ventricular internal dimension in diastrol (4.3 +/- 0.3 versus 4.3 +/- 0.5 cm) or systole (2.7 +/- 0.3 versus 2.6 +/- 0.4 cm), shortening fraction (0.37 +/- 0.05 versus 0.41 +/- 0.05), or mean normalized velocity of circumferential shortening (1.30 +/- 0.21 versus 1.31 +/- 0.23). Therefore, young, healthy women receiving oral contraceptives do not appear to be at increased risk with respect to abnormalities of ventricular volume or contraction.

Adolescent↗
PubMed1979

Ejection fraction derived by M-mode echocardiography: a table and comments.

Left ventricular ejection fraction is frequently quantitated by M-mode echocardiography despite limitations, including 1) the ability to measure an accurate left ventricular short axis, 2) the mathematic and geometric assumptions used to derive the volumes from which the ejection fraction is calculated, and 3) the lack of applicability to asynergic ventricles. Nevertheless, using a cubed function or correction formula, ejection fraction can be calculated for symmetrically contracting, normally sized, and enlarged left ventricles. A table and accompanying comments are presented.

Diastole↗
PubMed1979

Blood collection techniques, heparin and quinidine protein binding.

With the use of glass syringes without heparin and all glass equipment, the percent of unbound quinidine was measured by ultrafiltration and a double-extraction assay method after addition of 2 microgram/ml of quinidine sulfate. Compared to the all-glass method, collection of blood using Vacutainers resulted in an erroneous and variable decrease in quinidine binding related to blood to rubber-stopper contact. With glass, the unbound quinidine fraction was (mean +/- standard error) 10 +/- 1% in 10 normal volunteers, 8.5 +/- 1.5% in 10 patients with congestive heart failure, and 11 +/- 2% in 11 patients with chronic renal failure (although in 8 of the latter 11 patients the percent of unbound quinidine was 4 or more standard errors from the mean of the normal group). During cardiac catheterization, patients had markedly elevated unbound quinidine fractions: 24 +/- 2% (p less than 0.001). This abnormality coincided with the addition of heparin in vivo and was less apparent after the addition of up to 10 U/ml of heparin in vitro (120% and 29% increase in unbound quinidine fractions, respectively). Quinidine binding should be measured with all glass or equivalent equipment.

Blood Proteins↗
PubMed1978

Quinidine pharmacokinetics in patients with cirrhosis or receiving propranolol.

Quinidine pharmacokinetics (half-life, volume of distribution, and clearance) as well as protein binding were evaluated following a single 200 mg. oral dose of quinidine sulfate in eight control patients, in eight patients with moderate to severe cirrhosis, and in seven patients receiving 40 to 400 mg./day of propranolol. Patients with cirrhosis had a significantly longer quinidine half-life (9 +/- 1 hr; p less than .01) when compared to control patients (6 +/- 0.5h). This was not related to a reduced quinidine clearance rate but rather to an increase in quinidine volume of distribution (4.1 +/- .4 L./Kg. in cirrhotic patients vs 2.6 +/- 1 L./Kg. in control patients; p less than .01). Abnormal quinidine binding (greater than 25 per cent unbound fraction) was noted in seven of the eight cirrhotic patients. In contrast, patients receiving propranolol had a normal quinidine half-life of 6 +/- 0.5 hr. However, these patients had a significantly reduced quinidine clearance (3.3 +/- .7 ml./min./Kg. vs. 5.3 +/- .5 ml./min./Kg. in controls; p less than .05) and higher peak concentrations (1.25 +/- .20 micrograms/ml. vs. .80 +/- .5 micrograms/ml. in controls; p less than .05). Therefore in patients receiving propranolol, quinidine levels may be higher than expected shortly after dosage, and therefore a potential for transient toxicity exists in these patients. Maintenance quinidine dosage may have to be reduced in patients with moderate to severe hepatic cirrhosis, but not in patients receiving propranolol. Total quinidine concentration measurement underestimate free quinidine concentrations in most cirrhotic patients.

Adult↗