Dyspnea and left atrial myxoma.
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Dyspnea↗
Biomedical subjects
G Keren
Publications and source records attributed to G Keren.
Effects of an angiotensin II antagonist on ischemic and nonischemic isolated rat hearts.
BACKGROUND: Increasing evidence suggests that a locally integrated or intramyocardial renin-angiotensin system plays a significant role in ischemia-reperfusion injury. We evaluated the effects of losartan, an angiotensin II type 1 receptor blocking agent, on ischemic and nonischemic isolated rat hearts. METHODS: Using the modified Langendorff model, hearts were perfused with either low or high doses of losartan (18.2 mmol/L or 182.2 mmol/L, respectively) or with saline added to Krebs-Henseleit solution during phase I of the study. During phase II, hearts were exposed to a 60-minute period of global ischemia. Ischemic arrest was induced with warm cardioplegic solution (KCl, 16 mEq/L) containing either high-dose losartan (182.2 mmol/L) or Krebs-Henseleit solution only. RESULTS: During phase I of the study, no statistically significant differences were observed between the low-dose losartan group and the control group. However, hearts treated with high-dose losartan demonstrated an increase in peak systolic pressure, maximum first derivative of pressure, pressure-time integral, coronary flow, and oxygen consumption (p < 0.0001). During phase II, hearts treated with losartan showed a significantly better recovery on reperfusion, as reflected by better contractility (p < 0.001), higher oxygen consumption (p < 0.001), higher coronary flow (p < 0.0001), and lower creatine phosphokinase levels (41.1 +/- 1.7 versus 73.3 +/- 5.6 U/L; p < 0.001). CONCLUSIONS: High doses of losartan have a positive inotropic effect on normally perfused hearts. Given in cardioplegic solution, the drug has a significant protective effect on ischemic isolated rat hearts.
Angiotensin II↗
Fractal organization of the pointwise correlation dimension of the heart rate.
OBJECTIVE: To depict and quantify the degree of organization of the heart rate variability (HRV) in normal subjects. METHODS: A modified algorithm was created to estimate series of 'point-dimensions' (PD2) from interbeat (R-R) interval series of 10 healthy subjects (21-56 years). Our innovation is twofold: (i) we quantified instances of low-dimensional chaos, random fluctuations, and those for which our method failed to provide either (due to poor statistics); (ii) consecutive subepochs of PD2s underwent a relative dispersion (RD) analysis, yielding an index (D) which quantifies the dynamical organization of the heart rate generator. RESULTS: The mean values of PD2 series varied between 4.58 and 5.88 (mean+/-SD= 5.21+/-0.41, n = 10). For group 1 (21-30 years, n = 6) we found an averaged PD2 of 5.49+/-0.27, while for group 2 (47-56 years, n = 4) PD2 averaged 4.79+/-0.17. The RD analysis performed for subepochs of PD2s yielded both instances obeying fractal scaling (D < 1.5) and stochasticity (D > 1.5). The average D for group 1 was 1.39+/-0.04 (14 subepochs) and for group 2, 1.20+/-0.008 (8 subepochs). Paired t-test and Hartley F-max test for comparison between D values and homogeneity of variance between the two groups were performed, yielding P-values 0.004 and 0.02, respectively. CONCLUSIONS: The complexity of the HRV seems to be modulated by a non-random fractal mechanism of a 'hyperchaotic' system, i.e. it can be hypothesized to contain more than one attractor. Also, our results support the 'chaos hypothesis' put forth recently, namely, the complexity of the cardiovascular dynamics is reduced with aging. The index of relative dispersion of the dimensional complexity has to be tested in various clinico-pathological settings, in order to corroborate its value as a potential new physiological measure.
Adult↗
Angiographic Morphology Following Heparin and Aspirin Therapy in Patients with Acute Coronary Syndromes and Intracoronary Thrombus.
This series included 26 patients with acute myocardial infarction (15 patients) or unstable angina (11 patients), with thrombotic lesions identified by angiography and treated with intravenous heparin (mean 8 +/- 3 days, aPTT 1.5-2.5 times baseline) and aspirin (250 mg/day). A quantitative angiographic analysis was performed, and comparison of the lesion morphology before and after the antithrombotic treatment was conducted, using a computer-based analysis of the lesion contour. On average, minimal lumen diameter increased by 15.6% (1.15 +/- 0.5mm to 1.33 +/- 0.5mm, P = 0.02), percent diameter stenosis decreased by 10.7% (60.0 +/- 18% to 53.6 +/- 19%, P = 0.009), percent area stenosis decreased by 6.5% (80.0 +/- 14% to 74.8 +/- 16%, P = 0.05), and TIMI flow increased by 8% (2.5 +/- 0.9 to 2.7 +/- 0.7, P = 0.02). A significant improvement in the lesion morphology was more often observed in the right coronary artery (n = 9), than the left coronary artery (n = 16). We conclude that heparin and aspirin therapy improves the angiographic morphology and TIMI flow of thrombotic lesions in patients sustaining the acute coronary syndrome. This improvement was primarily found when the lesion was located in the right coronary artery.
Journal Article↗
High-dose intravenous gamma-globulins for heparin-induced thrombocytopenia: a prompt response.
Heparin-induced thrombocytopenia (HIT) is a common drug induced autoimmune condition. The thrombocytopenia is caused in most cases by an antibody directed against the complex PF4/heparin. Recently, we have induced an experimental model of HIT by idiotypic manipulation. To confirm further the idiotypic involvement of HIT, we have treated successfully three patients with HIT with high-dose intravenous gamma-globulin (IVIG). Our three patients joint other two cases previously reported who were treated with IVIG and point to the efficacy of this type of therapy with minimal side effects. IVIG suppression of the anti-PF4/heparin autoantibody may support the idiotypic etiology of HIT.
Aged↗
Hemodynamic changes determine the efficacy of thrombolysis: results from an in-vitro flow model.
BACKGROUND: The efficacy of thrombolytic therapy might be influenced by changes in the hemodynamic status. The aim of the study was to examine whether changes in perfusion pressure could affect the time to reflow in an in-vitro model. METHODS: The in-vitro flow system comprised flexible plastic tubes that enclosed a blood clot formed in one of the circuit arms. Streptokinase (125,000 U) or saline (control) was injected from a proximal side branch to induce thrombolysis. The protocol comprised four treatments: A, perfusion pressure 150/90 mmHg with streptokinase infusion; B, perfusion pressure 150/90 mmHg with saline; C, perfusion pressure 120/60 mmHg with streptokinase; D, perfusion pressure 120/60 mmHg with saline. Reflow was defined as flow restoration determined by the ultrasonic flowmeter. RESULTS: Successful recanalization was obtained in six of six samples subjected to treatment A (100%), two of seven samples subjected to treatment B (28%), three of five samples subjected to treatment C (60%) and none of six samples subjected to treatment D (0%). Time to reflow was 23 +/- 11 min with treatment A, 76 +/- 24 min with treatment B, 66 +/- 25 min with treatment C, and > 90 min with treatment D. CONCLUSIONS: Our data suggest that the hemodynamic status determines the efficacy of streptokinase-induced thrombolysis, and that spontaneous clot lysis is more likely to occur at greater perfusion pressures. It is conceivable that the hypotensive reaction induced by streptokinase in the clinical setting may adversely affect angiographic patency, compared with that observed with other lytic agents such as tissue-type plasminogen activator.
Blood Pressure↗
Transient bradycardia induced by carotid sinus pressure increases outflow obstruction in hypertrophic obstructive cardiomyopathy but not in valvular aortic stenosis.
BACKGROUND: The murmur of hypertrophic obstructive cardiomyopathy (HOCM) increases in intensity in about 80% of those patients in whom carotid sinus pressure (CSP) slows the heart rate. This does not occur in valvular aortic stenosis (AS). STUDY OBJECTIVES, DESIGN, AND PATIENTS: It was hypothesized that left ventricular (LV) obstruction increases with CSP in HOCM and not in AS. Furthermore, it was not clear whether it was the sudden bradycardia or CSP itself that was responsible for the effect noted. Therefore, studies were performed using two different interventions: (1) Doppler echocardiography was performed before and during CSP in 36 HOCM patients and 21 AS patients; (2) two patients with DDD pacemakers and HOCM were examined before and after pacemaker rate slowing. Finally, atrial pacing was performed in three HOCM patients at catheterization, and atrial pacing was either slowed or stopped (without CSP). RESULTS: LV outflow velocity and pressure gradient increased in 28 of 30 HOCM patients (92%) in whom heart rate decreased with CSP. The peak instantaneous pressure gradient increased from 45+/-37 to 77+/-53 mm Hg (p<0.005), and the velocity contour became more typical of HOCM. The pressure gradient increased from 30 mm Hg to 64 and 81 mm Hg, respectively, in the two patients with DDD pacemakers after pacemaker rate slowing. Similar results were seen with slowing or cessation of atrial pacing at catheterization. In contrast, the pressure gradient increased in only three of 21 AS patients (14%), to 44+/-28 from 41+/-25 mm Hg, and remained unchanged in the other 18. CONCLUSION: This study shows that LV outflow velocity and pressure gradient increase markedly in most HOCM patients (92%) if CSP succeeds in slowing the heart rate, but not in patients with valvular AS. A similar effect is obtained by simply decreasing the atrial rate in patients with DDD or atrial pacemakers. This increase in outflow tract obstruction is sufficient to account for the increase in murmur intensity. Decreased afterload (secondary to greater aortic decompression with the longer diastole), increased intrinsic force of contraction with the bradycardia (the Woodworth effect), and Starling's law may play independent roles in the dynamic increase in obstruction observed during CSP in patients with HOCM. Worsening of mitral regurgitation was not clearly shown to contribute to the increase in murmur, but it cannot readily be ruled out.
Adult↗
Changes in hemostatic function at times of cyclic variation in occupational stress.
In this study we demonstrated, in the same healthy subjects, a significant elevation in coagulation factors VII and VIII, fibrinogen, thrombocyte count, and thrombin and adenosine diphosphate-induced platelet aggregation during a period of increased workload compared with a calm work period. These findings may add to the understanding of the mechanism that links mental stress to coronary disease.
Adult↗
Compensatory enlargement, remodeling, and restenosis.
Coronary atherosclerosis is associated with vessel remodeling and dilatation. Quantitative analysis of arterial morphometry documents that as the cross sectional area of the plaque increases within a diseased vessel segment, the outer wall of the artery expands in an attempt to compensate for the accumulation of plaque. This focal compensatory enlargement maintains cross sectional area at stenotic sites of arteries, and the angiographic appearance of the vessel may be normal, despite marked accumulation of atherosclerotic plaque. Compensatory enlargement may develop as a response to increased shear stress caused by atherosclerotic plaque in conjunction with endothelial dependent factors, or alternatively, due to medial attenuation with loss of underlying structural support. The mechanism of arterial remodeling plays an important role in the development of arterial restenosis late after balloon dilatation or other interventional modalities. Stents prevent the remodeling process and restenosis with stents is the result of a relatively uniform neointimal tissue proliferation throughout the stent. Endovascular stents induce tissue proliferation both within the endoluminal stent surface and in the tissue layers surrounding the metallic Palmaz-Schatz stent struts. The therapeutic goals to prevent restenosis have to be oriented towards prevention of acute recoil, reduction of intimal, medial and adventitial prolific response and the phenomenon of inadequate arterial remodeling.
Angioplasty, Balloon↗
The role of botulinum toxin in the treatment of lower limb spasticity in children with cerebral palsy--a pilot study.
The use of botulinum toxin in cerebral palsy is still experimental. We conducted a pilot clinical trial with botulinum toxin injections on 14 children with spastic cerebral palsy. All patients were mobile with dynamic contractures of the gastrocnemius-soleus muscles. The injections were monophasic in 9 patients and biphasic in 5 patients. Improvement in dorsiflexion, quality of gait and grade of independence were achieved in 3 patients; improvement in dorsilflexion and quality of gait were achieved in 6 patients. There was no significant change in quality of gait in 4 patients. The beneficial effect lasted 4-9 months (mean 6.7 months). A combined functional score given by the physicians, therapists and parents showed a marked improvement in 6 patients (42.9%), a mild improvement in 3 patients (21.4%) and no improvement in 5 patients (35.7%). Biphasic injections were slightly more effective than monophasic injections (p < 0.02). Adverse effects were usually mild. We conclude that botulinum toxin may be used for the reduction of spasticity in patients with cerebral palsy who have dynamic deformities of the ankle joints.
Activities of Daily Living↗
[Circumcision and urinary tract infections].
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Circumcision, Male↗
Reduction of reinfarction and angina with use of low-molecular-weight heparin therapy after streptokinase (and heparin) in acute myocardial infarction.
This study examined whether extending the anticoagulation effect of heparin by low-molecular-weight heparin (clexane) can prevent recurrent myocardial infarction (AMI) treated by streptokinase. On the fifth day after AMI and after heparin therapy cessation, 103 patients were randomly assigned to either treatment with low-molecular-weight heparin (40 mg subcutaneously per day for 25 days, n=43) or control (no treatment, n=60). All patients were followed carefully for 6 months after the infarction date. A total of 32 patients (31%) sustained a cardiac event during the 6-month observation period. There were 12 patients (20%) with reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during the first 30 days of the study (p=0.02). One additional patient sustained reinfarction at 3 months of followup in the control group, which yielded a total of 13 patients (21.6%) sustaining reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during 6 months of followup (p=0.01). Angina pectoris after AMI was diagnosed in 13 control patients (21.6%) versus 4 low-molecular-weight heparin-treated patients (9.3%) (p=0.078) during the study period. No major bleeding events were reported in either low-molecular-weight heparin-treated or control patients. Among patients with recently diagnosed AMI treated by streptokinase, extending the anticoagulant effect of heparin for 25 days may prevent recurrent coronary events for at least one month.
Adult↗
Cepstrum analysis of reflected pressure waves in stenosed arteries.
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Animals↗
The in-vitro anti-rickettsial activity of macrolides.
The anti-rickettsial activity of azithromycin and clarithromycin was studied in Vero cells. The rate of rickettsial inhibition-growth caused by both macrolides was determined using rickettsial counts and ELISA. Both macrolides inhibited > 50% the growth of Rickettsia conorii and Rickettsia typhi at concentrations of 1.0 and 0.1 mg/L, respectively. The growth of Coxiella burnetii was inhibited to a rate of > or = 50% at the concentrations of 0.01 and 1.0 mg/L of azithromycin and clarithromycin, respectively.
Animals↗
Enhancement of recombinant tissue-type plasminogen activator thrombolysis with a selective factor Xa inhibitor derived from the leech Hirudo medicinalis: comparison with heparin and hirudin in a rabbit thrombosis model.
OBJECTIVE: To compare the efficacy of Yagin, a factor Xa inhibitor derived from the leech Hirudo medicinalis, with those of heparin and hirudin as adjuncts to recombinant tissue-type plasminogen activator (rTPA) thrombolysis in a rabbit thrombosis model. METHODS: Thirty-one animals were allocated randomly to three groups, all administered four boluses of 0.25 mg/kg rTPA every 10 min for 30 min, 17 mg/kg aspirin intravenously, and heparin (as a 100 IU/kg bolus followed by infusion of 50 IU/kg heparin per h), hirudin (as a 2 mg/kg bolus followed by infusion of 1 mg/kg hirudin per h), or Yagin (as an 80 micrograms/kg bolus followed by infusion of 43 micrograms/kg Yagin per h). RESULTS: Administration of Yagin was associated with a significant acceleration of the reflow time, this time being 14.5 +/- 1.2 min with Yagin, 25.8 +/- 5.2 min with heparin (P < 0.0001, versus Yagin), and 28.7 +/- 16.0 min with hirudin (P = 0.012, versus Yagin). Overall patency did not differ significantly among the three groups. CONCLUSIONS: At the indicated single doses, inhibition of factor Xa by a relatively low concentration of Yagin was found to be superior than that with either heparin or hirudin for accelerating rTPA thrombolysis.
Animals↗
Load dependence of left atrial and left ventricular filling dynamics by transthoracic and transesophageal Doppler echocardiography.
This article evaluates the pattern and effect of varying loading conditions on pulmonary venous flow and transmitral flow obtained by transthoracic and transesophageal echocardiography. We have conducted a two-stage study. A transthoracic echocardiographic study was performed in 15 patients with coronary artery disease and preserved left ventricular function. The transesophageal approach was used before open heart surgery where hemodynamic conditions were invasively monitored. Sublingual nitroglycerin (NTG) was administered to lower systolic blood pressure (mean 18 mm Hg) and resulted in a significant decrease in the peak passive left ventricular diastolic filling velocity (E wave) from 72 +/- 23 to 49 +/- 16 cm/s without marked changes in pulmonary venous flow pattern. In the transesophageal part of the study, Doppler-derived systolic (J), diastolic (K), and retrograde (R) phases of pulmonary venous flow, and passive (E) and active (A) phases of mitral flow were measured. Hemodynamic data were obtained invasively. Loading conditions were increased by infusion of saline and phenylephrine and reduced by NTG. Increased preload resulted in an augmented mitral E wave, an increased J wave, and an increased retrograde flow wave from the pulmonary veins. These changes were reversed by reduction of preload with NTG. Monitoring mitral and pulmonary venous flow may provide a relatively noninvasive means to assess directional changes in left ventricular preload.
Aged↗
Safety of coronary ultrasound angioplasty: effects of sonication on intact canine coronary arteries.
The purpose of this work was to examine in vivo the safety of sonication in the coronary arteries in a live animal model. In intact dogs (n = 8), balloon dilatation was performed on the proximal left anterior descending artery (LAD) followed by sonication to the left circumflex artery (LCX) in power levels found to be optimal for thrombus ablation. Post-dilatation and post-ultrasound coronary angiography, echocardiography, histopathology, CK-MB, indices of hemolysis, and coagulation were compared. Sonication did not induce changes in the ECG or blood pressure. Coronary angiography revealed no adverse side effects or change in arterial diameter (2.3 +/- 0.7 vs. 2.4 +/- 0.3 mm). Echocardiography showed transient opacification of the myocardium. Histopathology revealed a comparable minimal degree of endothelial denudation. After sonication there were no changes in the level of CK-MB (312 +/- 168 vs. 283 +/- 207 IU), hemoglobin (11.3 +/- 0.9 vs. 12.7 +/- 1.1 gr%), haptoglobin (479 +/- 136 vs. 451 +/- 121 mg/dL), fibrinogen (142 +/- 18 vs. 165 +/- 28 mg%), partial thromboplastin time (17.3 +/- 3.2 vs. 17.6 +/- 3.4 sec), prothrombin time (13.3 +/- 7.8 vs. 11.5 +/- 2.9 sec), and degree of platelet aggregation (55 +/- 17 vs. 62 +/- 8%). Thus, the data suggest that transluminal coronary sonication exerts no overt adverse effects in vivo.
Angioplasty, Balloon↗
Right bundle branch block of unknown age in the setting of acute anterior myocardial infarction: an attempt to define who should be paced prophylactically.
It is widely accepted that patients presenting with acute anterior myocardial infarction and acute onset of right bundle branch block should be prophylactically paced in contrast with those who have a chronic bundle branch block. The admitting physician is faced with the dilemma of how to act if the age of this conduction disturbance is unknown. This problem has further intensified in recent years, with the introduction of thrombolytic treatment, where insertion of a central vascular line is associated with increased morbidity. The objectives of this study were to define clinical or electrocardiographic parameters that may help the admitting physician to decide whether patients presenting with an anterior wall myocardial infarction and a right bundle branch block of unknown age should be prophylactically paced. We examined prospectively the in-hospital clinical course of 39 consecutive patients presenting with an acute myocardial infarction in whom the age of a right bundle branch block upon admission was unknown (group C, n = 39) and compared with two similar groups of patients who presented with an acute right bundle branch block (group A, n = 38) and with a known chronic right bundle branch block (group B, n = 22). Thirty-three patients (33%) died, with cardiogenic shock being the leading cause of death in the entire population. Prophylactic pacing, which was carried out in 66% and 54% of patients in groups A and C, respectively, did not reduce mortality rates. No clinical or electrocardiographic variables on admission were predictive to support prophylactic pacing in group C. In 10 of 46 (22%) patients who were prophylactically paced with a transvenous electrode, the following complications attributed to the procedure were detected: (1) either rapid sustained ventricular tachycardia (during implantation) that was unresponsive to overdrive pacing, or ventricular fibrillation necessitating electrical defibrillation (4 patients); (2) recurrent episodes of rapid nonsustained ventricular tachycardia, which stopped only after the pacemaker was turned off (1 patient); (3) complete AV block (1 patient); (4) fever appearing on the third or fourth day after implantation (3 patients); and (4) a large hematoma in the groin in 1 patient who was treated with thrombolysis shortly before pacemaker electrode insertion. Thus, the complications of transvenous temporary pacing in the era of thrombolysis may outweight any theoretical advantage.
Acute Disease↗