Biomedical subjects
S Atar
Publications and source records attributed to S Atar.
Mitral annular calcification: a marker of severe coronary artery disease in patients under 65 years old.
BACKGROUND: Mitral annular calcification has been associated with various systemic and cardiac diseases, with a higher prevalence in women and patients over 70. A possible association between mitral annular calcification and coronary artery disease has recently been suggested. OBJECTIVE: To determine the prevalence of severe coronary artery disease in younger patients with mitral annular calcification. METHODS: Consecutive patients aged or= 70% stenosis of at least one major epicardial coronary artery. PATIENTS: 17 735 patients were screened. Of these, 6207 (35%) had mitral annular calcification and 885 (5%) were also <or= 65 years old; coronary angiography was done in 100 of the latter (64 men; 36 women), mainly for anginal symptoms or a positive stress test. A control group (n = 121; 88 men, 33 women) was identified from 2840 consecutive patients screened. There was no significant difference between the groups in patient characteristics, indication for angiography, or atherosclerotic risk factors. RESULTS: Angiography showed a higher prevalence of severe coronary artery disease in patients with mitral annular calcification than in those without (88% v 68%, p = 0.0004), and a higher prevalence of left main coronary artery disease (14% v 4%, p = 0.009) and triple vessel disease (54% v 33%, p = 0.002). The positive predictive value of mitral annular calcification for finding severe coronary artery disease was 92%. CONCLUSIONS: In patients aged <or= 65 years, mitral annular calcification is associated with an increased prevalence of severe obstructive coronary artery disease. It may serve as a useful echocardiographic marker for the presence of obstructive coronary artery disease, especially when associated with anginal symptoms.
Comparison of serous and bloody pericardial effusion as an ominous prognostic sign.
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Clinical picture: thrombus in the left atrial appendage.
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Association of mitral annulus calcification, aortic valve sclerosis and aortic root calcification with abnormal myocardial perfusion single photon emission tomography in subjects age < or =65 years old.
OBJECTIVES: We examined the hypothesis that mitral annulus calcification (MAC), aortic valve sclerosis (AVS) and aortic root calcification (ARC) are associated with coronary artery disease (CAD) in subjects age < or =65 years. BACKGROUND: Mitral annulus calcification, AVS and ARC frequently coexist and are associated with coronary risk factors and CAD in the elderly. METHODS: We studied 338 subjects age < or =65 years who underwent evaluation of chest pain with myocardial perfusion single photon emission computed tomography (SPECT) and a two-dimensional transthoracic echocardiogram for other indications. The association of MAC, AVS and ARC with abnormal SPECT was evaluated by using chi-square analyses and logistic regression analyses. RESULTS: Compared with no or one calcium deposit and no or one coronary risk factor other than diabetes, multiple (> or =2) calcium (or sclerosis) deposits with diabetes or multiple (> or =2) coronary risk factors were significantly associated with abnormal SPECT in women age < or =55 years old (odds ratio [OR], 20.00), in women age >55 years old (OR, 10.00) and in men age < or =55 years old (OR, 5.55). Multivariate analyses identified multiple calcium deposits as a significant predictor for an abnormal SPECT in women (p < 0.001), younger subjects age < or =55 years (p < 0.05) and the total group of subjects (p < 0.01). CONCLUSIONS: When coronary risk factors are also taken into consideration, the presence of multiple calcium deposits in the mitral annulus, aortic valve or aortic root appears to be a marker of CAD in men < or =55 years old and women.
Augmentation of in-vitro clot dissolution by low frequency high-intensity ultrasound combined with antiplatelet and antithrombotic drugs.
BACKGROUND: Glycoprotein IIb/IIIa antagonists and heparin are increasingly used for treatment of acute coronary syndromes. There is no data on the effect of these drugs on clot dissolution when combined with low frequency high-intensity ultrasonic energy. We examined a possible additive effect of low frequency high-intensity ultrasound with an antithrombotic, an antiplatelet and a fibrinolytic agent alone or in combinations for in vitro blood clot dissolution. METHODS: Human blood clots were incubated for 10', 15' and 30' in normal saline containing commonly used concentrations of heparin, tirofiban, t-PA and Optison (echocardiographic contrast agent) alone and in combinations. Clots were then randomly exposed to low frequency high-intensity ultrasound (27[emsp3 ]kHz) for 5 minutes. The percent difference in clot weight and the incremental effect of ultrasound energy were calculated. RESULTS: The most significant additive effect of ultrasound energy was detected with the combination of tirofiban and heparin (39+/-2% augmentation after 10' of incubation, p<0.0001). The greatest magnitude of percent clot weight reduction was observed with ultrasound energy combined with either t-PA alone (72+/-1% after 30' incubation, p=0.0016) or with the combination of t-PA, tirofiban, heparin and Optison (68+/-4% after 30' incubation, p=0.015). CONCLUSIONS: Application of low frequency high-intensity ultrasound has an additive effect to antiplatelet, antithrombotic and fibrinolytic drugs, specifically with the combination of tirofiban and heparin or with t-PA; this effect is observed after a short incubation period.
Noninvasive transthoracic low frequency ultrasound augments thrombolysis in a canine model of acute myocardial infarction--evaluation of the extent of ST-segment resolution.
BACKGROUND: Recently it has been demonstrated that transcutaneous delivery of ultrasound combined with tissue plasminogen activator (tPA) is more effective than tPA alone in recanalizing acutely thrombosed canine coronary arteries. In the present study, we investigated the incidence of partial (> or =50%) and complete (> or =70%) ST-segment elevation resolution in the precordial leads of dogs with experimental acute myocardial infarction that were treated with tissue plasminogen activator (tPA) alone or in combination with noninvasive transcutaneous delivery of high-intensity low frequency (27[emsp3 ]kHz) ultrasound. METHODS: Thrombotic coronary occlusions were induced in the midportion of left anterior descending (LAD) coronary artery by electrical injury in 24 dogs. All dogs were given intravenous heparin and tPA. Dogs were randomized to tPA alone (n=12) or combined tPA and adjunctive transcutaneous ultrasound (US) delivery (n=12). Electrocardiograms were recorded at 1) baseline, 2) after coronary occlusion just before initiation of therapy, 3) when coronary angiography showed recanalization of the coronary artery (or at 90 minutes after initiation of therapy if reperfusion did not occur before then) and 4) 90 minutes later. ST amplitude was measured in all 6 precordial leads. RESULTS: ST-segment amplitude at baseline was comparable between the tPA and the US group. Before initiation of therapy, sum of ST-segment elevation tended to be higher in the US group. At reperfusion and 90 minutes thereafter, sum of ST-segment amplitude tended to be smaller for the US group than in the tPA group (p<0.001 for the time effect; p=0.118 for the time x group interaction). Up to 90 minutes after initiation of therapy >/=50% resolution of the sum of precordial ST elevation was detected in 7 out of 11 dogs (63.6%) in the tPA group versus 10 out of 11 dogs (90.9%) in the US group. Ninety minutes thereafter, 3 out of 7 dogs in the tPA group (42.9%) versus 9 of 11 dogs in the US group (81.8%) had >/=50% resolution of the sum of precordial ST elevation. CONCLUSIONS: The combination of tPA with noninvasive transcutaneous delivery of low frequency high-intensity ultrasound resulted in greater resolution of ST-segment elevation when reperfusion occurs and 90 minutes thereafter, as well as a higher rate of epicardial coronary artery reperfusion.
The use of transducer-tipped ultrasound catheter for recanalization of thrombotic arterial occlusions.
Ultrasound energy is currently being used and intensively investigated for recanalization of thrombotically occluded arteries. The ultrasonic energy is mainly applied either by a transcutaneous approach or by a percutaneous approach through a catheter with an external ultrasound transducer. Catheter-delivered transducer-tipped ultrasound thrombolysis is a new and innovative method. In this article we summarize the current available data on the use of this new type of catheter and discuss future directions and clinical applications.
Noninvasive transcutaneous low frequency ultrasound enhances thrombolysis in peripheral and coronary arteries.
Previous studies have shown that external ultrasound with low frequencies and high intensities can enhance thrombolytic drug-induced clot dissolution during in vitro experiments. In this series of studies, we evaluated the efficacy of peripheral and coronary thrombolysis in vivo in animals by using noninvasive transcutaneous ultrasound combined with thrombolytic drugs (streptokinase and tPA) and/or microbubbles agents (dodecafluoropentane [DDFP] and perfluorocarbon-exposed sonicated dextrose albumin [PESDA]). Thrombotic occlusions were induced in 74 rabbit iliofemoral arteries and 24 canine left anterior descending (LAD) coronary arteries in this in vivo study. By using the combination of transcutaneous ultrasound and streptokinase, the angiographic patency rate in rabbit iliofemoral arteries was higher (56%-100%) than with ultrasound (6%; P < or = 0.0036) and streptokinase alone (6%; P < or = 0.0012). Also, with transcutaneous ultrasound and microbubbles, the angiographic patency rates were 76%-100% as compared with ultrasound alone (0%, P < or = 0.0003) or microbubbles alone (9%, P < or = 0.0001). In the canine study of acute myocardial infarction, thrombolysis in myocardial infarction (TIMI) grade flow at 90 minutes in the tPA alone group was 0.92 +/- 1.4 as compared with 2.42 +/- 1.9 in the tPA plus transthoracic ultrasound group (P = 0.006). There was much improved reperfusion with tPA plus ultrasound as compared with tPA alone. In vivo animal studies demonstrate that noninvasive transcutaneous ultrasound can greatly enhance the effect of clot dissolution with thrombolytic drugs and/or microbubbles, and has the potential for clinical application as an adjunctive method to improve arterial thrombolysis.
Arterial thrombus dissolution in vivo using a transducer-tipped, high-frequency ultrasound catheter and local low-dose urokinase delivery.
PURPOSE: To examine the hypothesis that a transducer-tipped high-frequency ultrasound drug-delivery catheter may augment the thrombolytic effects of locally delivered low-dose urokinase and result in improved recanalization rates and reduced residual thrombotic burden. METHODS: Thrombi were induced in situ bilaterally in 5- to 6-cm-long segments of the superficial femoral arteries in 9 dogs by intraluminal thermal damage and injection of thrombin. A transducer-tipped high-frequency local drug-delivery catheter was applied at 1.1 MHz and 0.6 W for 60 minutes to one superficial femoral artery segment, and an identical catheter with an inactivated ultrasound transducer was used to treat the contralateral control segment. Urokinase (5000 IU/kg) was delivered bilaterally into the thrombi during the treatment interval. RESULTS: Angiography documented TIMI grade 2 or 3 flow in 9 (100%) segments in the ultrasound-treated group versus 6 (67%) of the controls (no ultrasound) (p = 0.058). Angiographically detected distal embolization was found in 2 ultrasound-treated segments compared with 5 controls (p = 0.02). Protruding or occlusive thrombi were seen angioscopically in 8 (89%) control segments but in only 1 (11%) of the ultrasound-treated arteries (p < 0.001). By histopathology, 7 (78%) segments in the control group had occlusive thrombi, whereas only 3 nonocclusive thrombi were found in the ultrasound-treatment group (p < 0.001). CONCLUSIONS: Catheter-delivered high-frequency ultrasound and local low-dose urokinase infusion is efficacious for the treatment of acute thrombotic occlusions as evaluated by angiography, angioscopy, and histopathology.
"Cyanotic blue tongue" in severe rheumatic tricuspid regurgitation.
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Pacing stress echocardiography: an alternative to pharmacologic stress testing.
OBJECTIVES: We sought to evaluate the diagnostic accuracy and feasibility of bedside pacing stress echocardiography (PASE) as a potential substitute for pharmacologic stress echocardiography in patients admitted to the hospital with new-onset chest pain or worsening angina pectoris. BACKGROUND: Accurate and rapid noninvasive identification and evaluation of the extent of coronary artery disease (CAD) is essential for optimal management of these patients. METHODS: Bedside transthoracic stress echocardiography was performed in 54 consecutive patients admitted to a community hospital with new-onset chest pain, after acute myocardial infarction had been excluded. We used 10F transesophageal pacing catheters and a rapid and modified pacing protocol. The PASE results were validated in all patients by coronary angiography performed within 24 h of the test. Significant CAD was defined as > or =75% stenosis in at least one major epicardial coronary artery. RESULTS: The sensitivity of PASE for identifying patients with significant CAD was 95%, specificity was 87% and accuracy was 92%. The extent of significant CAD (single- or multivessel disease) was highly concordant with coronary angiography (kappa = 0.73, p<0.001). Pacing stress echocardiography was well tolerated, and only 4% of the patients had minor adverse events. The mean rate-pressure product at peak pacing was 22,313+/-5,357 beats/min per mm Hg, and heart rate >85% of the age-predicted target was achieved in 94% of patients. The average duration of the bedside PASE test, including image interpretation, was 38+/-6 min. CONCLUSIONS: Bedside PASE is rapid, tolerable and accurate for identification of significant CAD in patients admitted to the hospital with new-onset chest pain or worsening angina pectoris.
Transthoracic stress echocardiography with transesophageal atrial pacing for bedside evaluation of inducible myocardial ischemia in patients with new-onset chest pain.
To date, there are no data on the feasibility and accuracy of bedside pacing stress echocardiography in patients admitted to the hospital with new-onset chest pain or unstable angina. We evaluated the feasibility of pacing stress echocardiography and examined its correlation with myocardial perfusion stress scintigraphy (rest thallium-201/stress technetium-99m sestamibi dual-isotope myocardial perfusion single-photon emission computerized tomography) performed within 24 hours of the pacing stress echocardiography test. We studied 70 consecutive patients after acute myocardial infarction had been excluded. The bedside pacing stress echocardiography test was performed with 10Fr transesophageal pacing catheters. We found pacing stress echocardiography to be feasible and safe (3% minor adverse event rate) at the patients' bedside. Target heart rate of >85% of the age-predicted heart rate was achieved in 96% of patients, and the mean rate-pressure product was 22,644 +/- 4,520 beats/min/mm Hg. The mean duration of the bedside pacing stress echocardiography test including technical preparations and image interpretation was 41 +/- 7 minutes. Pacing stress echocardiography and myocardial perfusion stress scintigraphy correlated well for identification or exclusion of inducible myocardial ischemia in 63 of 70 patients (90%) (kappa 0.81, p <0.001). The extent of inducible myocardial ischemia by vascular territories correlated with myocardial perfusion stress scintigraphy in 52 of 70 patients (74%) (kappa 0.6, p <0.001). We conclude that bedside pacing stress echocardiography is feasible and safe, and highly correlates with myocardial perfusion stress scintigraphy for identifying inducible myocardial ischemia in patients with new onset of chest pain or unstable angina.
Microparticle-containing oncotic solutions augment in-vitro clot disruption by ultrasound.
Echocardiographic contrast agents enhance blood clot disruption by ultrasound. It has been suggested that the microbubbles add nuclei for the enhancement of cavitation by ultrasound. However, microbubbles are rapidly destroyed by the ultrasound energy. We assessed whether non-gas filled colloidal solutions (hyperoncotic medium molecular hydroxyethyl starch and degraded gelatin polypeptides) will facilitate clot disruption by ultrasound. In two separate experiments human blood clots, 200-400 mg in weight, were weighed and then immersed for 15 seconds in 10 ml normal saline solution containing 0%, 0.1%, 1%, 2%, and 5% of hyperoncotic medium molecular hydroxyethyl starch or 0%, 0.035%, 0.175%, 0.35%, and 0.7% degraded gelatin polypeptides. Clots were randomized to 10 seconds 20 kHz ultrasound or immersion without ultrasound. After treatment, the clots were reweighed, and the percent difference in weight was calculated. Non-gas filled microparticle-containing solutions such as hyperoncotic medium molecular hydroxyethyl starch and degraded gelatin polypeptides significantly augmented blood clot disruption by ultrasound. The effect is dependent on the colloidal solution concentration with maximal effect achieved with 1% hyperoncotic medium molecular hydroxyethyl starch and 0.35% degraded gelatin polypeptides.
Noninvasive, transthoracic, low-frequency ultrasound augments thrombolysis in a canine model of acute myocardial infarction.
BACKGROUND: Limitations of coronary thrombolysis include the time to reperfusion, patency rate, and bleeding. We evaluated the use of noninvasive transcutaneous ultrasound to augment coronary thrombolysis. METHODS AND RESULTS: In 24 dogs, a thrombotic occlusion of the left anterior descending coronary artery was induced and documented by 12-lead ECG and coronary angiography. After >/=60 minutes of occlusion, tissue-type plasminogen activator (t-PA; 1.42 mg/kg) was given intravenously over 90 minutes. A total of 12 of the 24 dogs had concomitant transcutaneous application of low-frequency ultrasound (27 kHz) over the chest. At 90 minutes, the mean TIMI grade flow in the t-PA alone group was 0.92+/-1.4 compared with 2. 42+/-1.9 in the t-PA plus ultrasound group (P=0.006). TIMI 2 to 3 flow was present in 4 of 12 cases receiving t-PA alone compared with 10 of 12 cases receiving t-PA plus ultrasound (P=0.003). At 180 minutes, mean TIMI grade flow was 0.75+/-1.4 in the t-PA alone group versus 2.58+/-0.9 in the t-PA plus ultrasound group (P=0.001). Pathological examination confirmed the angiographic patency rate and did not reveal injury secondary to ultrasound in the skin, soft tissues, heart, or lungs. CONCLUSIONS: In vivo, the noninvasive transthoracic application of low-frequency ultrasound (1) greatly augments the efficacy of t-PA-mediated thrombolysis, (2) seems safe, and (3) has substantial potential as a noninvasive adjunct to improve coronary patency without increasing the risk of bleeding.
Tricuspid valve group B streptococcal endocarditis after an elective termination of pregnancy.
A patient developed fever, chills, and shortness of breath after an elective first trimester dilation and curettage. Blood cultures grew Group B streptococcus, and a transesophageal echocardiogram revealed a 2 x 2 cm vegetation on the tricuspid valve and global left ventricular hypokinesis. A 6-week course of parenteral antibiotics and vasodilator therapy resulted in resolution of the valvular vegetation as well as of the left ventricular dysfunction.
Ultrasound has synergistic effects in vitro with tirofiban and heparin for thrombus dissolution.
Previous studies have shown synergism between ultrasound and thrombolytic agents or microbubbles on blood clot dissolution. It has not been investigated whether heparin or glycoprotein IIb/IIIa blockers enhance clot lysis by ultrasound. We compared the blood clot dissolution effect of saline, heparin, tissue plasminogen activator (tPA), tirofiban, and an echocardiographic contrast media (Optison) without and with ultrasound application. Human blood clots from four donors, 2 to 4 hours old, were cut into 200- to 400-mg sections, weighed, and immersed for 2 minutes in 1 L of normal saline 0.9% solution containing either heparin 1000 U, tirofiban 150 microg, tPA 20 mg, Optison 0.5 mL, or normal saline alone. Clots were randomized to 2 minutes ultrasound application or immersion alone without ultrasound. Ultrasound was applied with a 19.5 KHz catheter. After treatment, the clots were weighed, and the absolute and percent difference in weight was calculated. Immersion in heparin, tirofiban, and tPA without ultrasound did not augment clot disruption relative to normal saline alone. Immersion in Optison (p = 0.07) tended to result in less lysis than saline alone. Ultrasound enhanced clot dissolution compared to immersion alone with: saline (48.1+/-15.3% vs. 26.0+/-13.8%, p<0.0000002); heparin (60.8+/-17.5% vs. 30.8+/-15.1%, p = 0.000001); tirofiban (61.8+/-13.6% vs. 30.1+/-12.2%, p<0.0000001); tPA (53.1+/-15.3% vs. 30.2+/-11.5%, p<0.000002); and Optison (47.8+/-16.0% vs. 18.4+/-11.5%, p<0.0000001). The combination of tirofiban with ultrasound, as well as heparin with ultrasound, was associated with a significant augmentation of clot dissolution compared with the saline plus ultrasound group (p = 0.002, 0.013, respectively). Ultrasound with tPA or with Optison had no significant augmentation of clot dissolution over the ultrasound + saline effect. This in vitro study of catheter-delivered high-intensity low-frequency ultrasound demonstrates that: (1) tirofiban and heparin, as well as perfluorocarbon microbubbles, augment clot dissolution by ultrasound; (2) augmentation of clot dissolution is evident even after only brief exposure of ultrasound and the drug studied.
Transesophageal echocardiographic Doppler findings in patients with penetrating aortic ulcers.
Penetrating aortic ulcers and intramural hematomas cannot always be differentiated by transesophageal echocardiography. We suggest that color and pulsed-wave Doppler flow can be used for identifying penetrating aortic ulcers.