Biomedical subjects
Publications and source records attributed to G Keren.
Cryptosporidium infection in immunocompetent patients has been described as a mild self-limiting diarrhoea. We describe two immunocompetent infants presented with life-threatening protracted diarrhoea. These two cases expand on the clinical spectrum of cryptosporidiosis in normal hosts.
The present study was designed to assess the relative contribution of atrial fibrillation and left atrial pressure to changes in the size of the left and right atria in patients with mitral stenosis. The study included 155 subjects, 102 of whom underwent prospective echocardiography and Doppler cardiography, and 69 of whom underwent cardiac catheterization. The size of the atria was determined by two-dimensional echocardiography. There were no significant hemodynamic differences between patients with mitral stenosis who were in either sinus rhythm or atrial fibrillation. The left atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (37.6 +/- 10.8 cm2) than in patients in sinus rhythm (27.8 +/- 7.7 cm2) or normal subjects (15 +/- 3.3 cm2). The size of the right atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (21.7 +/- 5.2 cm2) than in patients in sinus rhythm (13.4 +/- 3.9 cm2) or normal subjects (13.8 +/- 3.7 cm2). Multiple regression analysis showed that the severity of mitral stenosis accounted for 38%, age for 7%, and atrial fibrillation for 11% of the change in the size of the left atrium. Atrial fibrillation accounted for 24%, age for 11, and mitral valve area for 3% of the change in the size of the right atrium. The analysis suggests that the onset of left atrial dilatation in mitral stenosis is the result of an early increase in left atrial pressure. Atrial fibrillation, which develops irrespective of the severity of the mitral stenosis, contributes to a further enlargement of the left and right atria.
We examined the hemodynamic effects of congesting cuffs (rotating tourniquets) in 12 patients with first acute myocardial infarction and new onset of congestive heart failure 24 to 48 hours after admission. Congesting cuffs were applied for two periods of 15 minutes each, 15 minutes apart, and inflated to 30 mm Hg and 60 mm Hg consecutively. No change was noticed in mean pulmonary artery wedge pressure, which was 20 +/- 3 mm Hg at the beginning of the study and 19 +/- 3 mm Hg at the completion (P greater than .05, NS), nor in other hemodynamic and blood gases parameters. Patients' clinical conditions remained unchanged. We conclude that application of congesting cuffs at pressures of 30 mm Hg and 60 mm Hg does not result in any change in clinical or hemodynamic data in patients with acute myocardial infarction and new onset of congestive heart failure.
Sixteen patients with acute myocardial infarction underwent treatment with streptokinase up to 3 hours after the onset of chest pain. Nine patients (group I) received streptokinase within 1 hour of the onset of pain, and seven patients (group II) received it within 2 to 3 hours. All underwent multigated radionuclide ventriculography after streptokinase therapy and 1 week later. Percutaneous transluminal coronary angioplasty of the infarct artery was performed within 24 hours in all patients. An effort-limited treadmill stress test was performed before discharge. There was no mortality or serious complication. Mean peak total creatine kinase was 521 +/- 289 mU/ml in group I, and 1,614 +/- 709 mU/ml in group II (p less than 0.05). The mean initial left ventricular ejection fraction was 47 +/- 11% in group I and 37 +/- 10% in group II. After early angioplasty (within 24 hours) and at 1 week recovery, left ventricular ejection fraction increased to 53 +/- 9% in group I (p less than 0.05) and to 40 +/- 7% in group II (p = NS). Seven of the nine patients in group I had normal radionuclide ventriculograms at discharge compared with none of the seven patients in group II. Thrombolytic therapy administered less than 1 hour after the onset of symptoms of acute myocardial infarction followed by angioplasty of the infarct artery results in preservation of left ventricular function, whereas therapy given after 2 hours has only a limited effect.
Forty-six episodes of cerebrospinal fluid shunt infections developed in 32 patients undergoing cerebrospinal fluid shunt operations during a 13-year period (1972 to 1984). The infection rate was 21%/operative procedure and 33%/patient. The shunt infection rate in revisions of infected shunts was 52%, a rate significantly larger than that in revisions of noninfected shunts (11%). Eight patients (25%) of the initially infected patients had more than one infectious episode. Predominating pathogens in patients who had shunt revisions included coagulase-negative staphylococci in 8 of 15 episodes (4 patients). Coagulase-negative staphylococci accounted for 28% and coagulase-positive staphylococci for 14% of the initial infectious episodes. Risk factors for development of shunt infection included age younger than 3 years, a previously infected shunt and surgery to revise the infected shunt. Therapy of infected shunts with antibiotics alone or with antibiotics plus an operative shunt revision resulted in similar success rates.
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Serious infectious complications of open-heart surgery in 521 adults who underwent 534 open-heart procedures are reviewed. Bacteremia complicated seven (1.3%) of the procedures, carditis six (1.1%) and deep sternal wound infections nine (1.7%). The overall rate of these infections was 4.1% with an associated death rate of 11.7% (2 of 17). With respect to the risk of this complication, no differences were noted in the age of the patients, duration of surgery or perioperative prophylaxis with cephalothin or cloxacillin. The chance of carditis developing was significantly related (p less than 0.001) to a valve replacement procedure and the risk of a deep sternal wound infection (p less than 0.01) to a procedure classed as "other". Staphylococci remained the most commonly isolated pathogens with an almost equal frequency of Staphylococcus epidermidis and Staphylococcus aureus. Gram-negative aerobes and Streptococcus faecalis were found to be other important pathogens in this clinical setting.
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The in vitro activity of ofloxacin, a new quinolone derivative, was compared to that of other agents commonly in use against pathogens isolated in the community and in the hospital. None of the community or hospital strains isolated from urinary tract infection showed resistance to ofloxacin, while variable resistance was demonstrable with all other oral agents. Similar results were obtained with pathogens isolated from infected wounds originating in the community and in the hospital. Among pathogens isolated from the respiratory tract, ofloxacin was most active against Haemophilus influenzae, but less active than the penicillin-cephalosporin group against Streptococcus pneumoniae. Ofloxacin was active against all but one (Pseudomonas aeruginosa) blood culture isolates. Of 112 strains isolated from community-acquired infections, only one strain was ofloxacin-resistant while resistance to sulphamethoxazole-trimethoprim, ampicillin and doxycycline was 34%, 42% and 30%, respectively. Among 219 pathogens originating from nosocomial infections, 3.2% were resistant to ofloxacin compared to 56% for cefazolin, to 7.2% for cefotaxime, 15.8% for piperacillin and 22.3% for gentamicin. These results suggest that ofloxacin has great therapeutic potential for the therapy of bacterial infections originating both in the community and in the hospital.
Seven patients with decompensated chronic heart failure and functional mitral regurgitation were studied before and during administration of nitroglycerin at a mean dose of 42 micrograms/min (range 20 to 90 micrograms/min). Forward aortic flow obtained by pulsed Doppler increased significantly from 35 +/- 8 to 45 +/- 9 ml/beat (p less than 0.001) and correlated well with the cardiac output measured by thermodilution technique (r = 0.8). Whereas regurgitant mitral volume calculated from the difference between echocardiographic total stroke volume and forward aortic flow decreased significantly from 19 +/- 9 to 3 +/- 3 ml/beat (p less than 0.001), peak velocity of mitral regurgitant flow increased from 4.1 +/- 0.9 to 4.4 +/- 1.0 m/sec (p less than 0.05). The decrease in effective mitral regurgitation area derived from a modified Gorlin formula average 80%. Accordingly, in patients with decompensated chronic heart failure and functional mitral regurgitation, nitroglycerin decreases mitral regurgitant area substantially, and thus almost abolishes mitral regurgitation despite an increase in systolic pressure gradient between left ventricle and atrium. Moreover, the increase in forward flow can be entirely accounted for by the reduction in mitral regurgitant flow.
Syncope is a rare presentation of glossopharyngeal neuralgia (GN). The mechanisms of the syncope were studied in a patient with recurrent episodes comprising prolonged cardiac standstill and arterial hypotension. During attacks, no supraventricular or ventricular potentials were recorded in the ECG. Atropine prevented the cardiac arrest without affecting the pain, indicating the vagus as the efferent limb of the reflex asystole. Following atropine blood pressure continued to fall during GN attacks, suggesting abolition of sympathetic tone. Indeed, serum norepinephrine levels fell during these attacks. Infiltration of either vagus above the clavicle with local anesthetics did not abolish the cardiac asystole. Carbamazepine and a dual chamber pacemaker were effective in controlling the symptoms of the patient. The results suggest that, during a neuralgic attack, the stimulation excites both vagi, causing asystole and simultaneously abolishes sympathetic tone.
Pulmonary venous flow has two phases (systolic and diastolic) in normal subjects when studied by pulsed Doppler echocardiography. Only one phase of pulmonary venous flow (diastolic) was observed in six patients without synchronous atrial contraction (four patients with atrial fibrillation and two with complete atrioventricular [AV] block). This pattern reversed to normal (biphasic) when AV synchrony was reestablished by cardioversion to sinus rhythm in patients with atrial fibrillation and by AV sequential pacing in patients with complete AV block. Thus, both atrial and ventricular contraction and relaxation are important determinants of pulmonary venous flow.
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This study offers a unifying mechanism of left ventricular filling dynamics to link the unexplained mid-diastolic motion of the mitral valve with an associated increase in transmitral flow, with the phasic character of pulmonary vein flow, and with changes in the atrioventricular pressure difference. M mode echograms of mitral valve motion and Doppler echocardiograms of mitral and pulmonary vein flow velocities were recorded in 12 healthy volunteers (heart rate = 60 +/- 9 beats/min). All echocardiograms showed an undulation in the mitral valve (L motion) at a relatively constant delay from the peak of the diastolic phase of pulmonary vein flow (K phase). In six subjects, the L motion was also associated with a distinct wave of mitral flow (L wave). Measured from the onset of the QRS complex, Q-K was 577 +/- 39 msec; Q-L was 703 +/- 42 msec, and K-L was 125 +/- 16 msec. Multiple measurements within each subject during respiratory variations in RR interval indicated exceptionally small differences in the temporal relationships (mean coefficient of variation 2%). Early rapid flow deceleration is caused by a reversal of the atrioventricular pressure gradient, and the L wave arises from the subsequent reestablishment of a positive gradient due to left atrial filling via the pulmonary veins. The mitral valve moves passively in response to the flowing blood and the associated pressure difference. This interpretation is confirmed by (1) a computational model, and (2) a retrospective analysis of data from patients with mitral stenosis and from conscious dogs instrumented to measure transmitral pressure-flow relationships.
Angiographic results in patients with mitral regurgitation suggest that up to 50% of the regurgitant volume occurs during the preejection period. This contrasts markedly with the electromagnetic measurements of mitral regurgitant flow in anesthetized dogs, which suggest that only 5% of mitral regurgitant flow occurs during the preejection period. Therefore, we used two-dimensional and Doppler echocardiography to quantify mitral regurgitation during aortic ejection and in the preejection and postejection periods in eight patients with severe heart failure. Mitral regurgitant volume (RV) was calculated as the difference between total stroke volume (by two-dimensional echocardiography) and forward aortic flow (by pulsed Doppler). Regurgitant velocity (V) and time (RT) were measured by continuous-wave Doppler, and the mean regurgitant area (RAm) was calculated from the RT and mean regurgitant velocity (Vm): RAm = (RV/RT)/Vm. As a first approximation, the RA was assumed to be constant during systole, and the regurgitant volume during aortic ejection and during the preejection and postejection periods was calculated from: RVi = (Vmi) (RTi) (TAm), where Ti represents the duration of the appropriate period. Percentages of total regurgitant volume occurring during the preejection, ejection, and postejection periods were 13 +/- 4%, 79 +/- 5%, and 8 +/- 5%, respectively. Thus, in contrast to previously reported angiographic studies, mitral regurgitation occurs predominantly during the aortic ejection period. These results were not substantially changed by assuming a 20% reduction in effective regurgitant orifice area between the preejection and ejection periods and are consistent with data from chronically instrumented dogs with mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
While the acute hemodynamic efficacy and safety of the novel inotropic agents are well recognized, their long-term effects on symptoms, quality of life, and survival, in patients with chronic congestive heart failure, are controversial. Such controversy may result from a poor understanding of the disease process and its progression, unrealistic expectations on the potential benefits of enhancing myocardial contractility at an advanced stage of the disease, and the lack of knowledge of the precise mechanisms of action of the novel inotropic agents. To put into perspective the role of the novel inotropic agents in the treatment of chronic congestive heart failure, the effects of dobutamine (a synthetic catecholamine which is the most potent inotropic agent currently available) were reviewed. Changes in cardiac performance, myocardial contractility and metabolism, and exercise capacity were studied in patients with chronic congestive heart failure of variable severity. The acute hemodynamic effects and the mechanism of action of the novel inotropic agents were then reviewed and compared to those of dobutamine. Which patients with chronic congestive heart failure who are the most likely to benefit from therapy with the novel inotropic agents, and the therapeutic limitations of these agents are discussed. Lastly, the difficulties of selecting the right endpoints to demonstrate the long-term efficacy of the novel inotropic agents are considered.
An adult patient with isolated septic arthritis of the sternoclavicular joint (SCJ) caused by Staphylococcus aureus is described. The patient had no underlying diseases other than paronychia, which might have served as the portal of entry. Antibiotic therapy resulted in clinical cure but x-ray revealed progression of the destructive process.