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Objectives: To evaluate the usefulness of a novel qualitative, rapid, bedside immunoassay device for the detection of elevated creatine kinase MBmass (CK-MB) and myoglobin as a supportive tool for decision-making by the physician who is evaluating patients who present with chest pain., Design: Prospective study., Setting: Prehospital (mobile intensive care units)., Patients: Three hundred twenty-eight consecutive patients, age 71+/-13 yrs (64% males), who were admitted to the hospital via Shahal's mobile intensive care units., Intervention: During a 6-month period, based on clinical presentations and electrocardiograms, the mobile's physicians classified patients into groups of high or low probability of having an acute myocardial infarction and, thereafter, used a rapid bedside STATus kit (Spectral Diagnostics, Toronto, Ontario, Canada) to determine blood creatine kinase/MB and myoglobin., Measurements and Main Results: Myocardial infarction was confirmed in 59 (18%) patients. If measured >2 hrs after onset, diagnostic sensitivities, specificities, and positive and negative predictive values for physicians were as follows: 71%, 90%, 46%, and 96%, respectively, compared with 100%, 85%, 44%, and 100%, respectively, if assessed by the kit., Conclusions: If used 2 to 12 hrs from the onset of symptoms, this device is a convenient diagnostic aid to prevent a misdiagnosis of acute myocardial infarction or unnecessary hospitalization to exclude infarction. This tool may be a promising cost-cutting factor in these days of escalating expenses and dwindling resources.

Background: Percutaneous transluminal treatment of a thrombotic vein graft yields poor results. We have previously reported our experience with transluminal percutaneous coronary ultrasound thrombolysis (CUT) in the setting of acute myocardial infarction (AMI). This report describes the first experience with ultrasound thrombolysis in thrombus-rich lesions in saphenous vein grafts (SVGs), most of which were occluded., Methods and Results: The patients (n=20) were mostly male (85%), aged 64+/-4 years old. The presenting symptom was AMI in 2 patients (10%) and unstable angina in the rest. Fifteen patients (75%) had totally occluded SVGs. The median age of clots was 6 days (range, 0 to 100 days). The ultrasound thrombolysis device has a 1.6-mm-long tip and fits into a 7F guiding catheter over a 0.014-in guidewire in a "rapid-exchange" system. CUT (41 kHz, 18 W,

Background: Atrioventricular nodal reentry tachycardia (AVNRT) represents the most commonly encountered type of regular paroxysmal supraventricular tachycardia. This study determined whether administration of adenosine-5'-triphosphate (ATP) during sinus rhythm may be useful in the noninvasive diagnosis of dual AV nodal pathways., Methods and Results: During electrophysiological study, we intravenously administered incremental doses of ATP (from 10 to 50 mg) during sinus rhythm to patients with spontaneous and inducible sustained AVNRT (study group, n=42) and to patients with no evidence of dual AV nodal physiology or inducible AVNRT (control group, n=21). Signs suggestive of dual AV node physiology after ATP administration during sinus rhythm ("jump" of AH > or =50 ms between 2 consecutive beats, > or =1 AV nodal echo beat, or initiation of AVNRT) were observed in 32 (76%) of 42 study patients but in only 1 (5%) of the 21 control patients (P<0.001). Similar results were observed when only surface lead recordings (without intracardiac recordings) were evaluated. Signs suggestive of dual AV node physiology by the ATP test were observed in 29 (80.5%) of 36 patients who had electrophysiological demonstration of dual AV node physiology and in 3 (50%) of 6 patients without AV nodal duality (P=NS). Signs suggestive of dual physiology according to the ATP test disappeared in 11 (92%) of the 12 patients who underwent successful slow AV nodal ablation but persisted in 8 (62%) of 13 patients who underwent AV nodal modification., Conclusions: Administration of ATP during sinus rhythm may be a useful bedside test for identifying patients with dual AV nodal pathways who are prone to AVNRT. This simple test should be considered as a screening test for patients with symptoms suggestive of paroxysmal supraventricular tachycardia but no documented arrhythmias or for patients with documented narrow complex tachycardia of unclear mechanism.

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.

Background: It has been demonstrated that therapeutic ultrasound effects ultrasound thrombolysis by selectively disrupting the fibrin matrix of the thrombus. This study was conducted to evaluate the clinical feasibility of percutaneous transluminal coronary ultrasound thrombolysis in acute myocardial infarction (AMI)., Methods and Results: Consecutive patients (n = 15) with evidence of anterior AMI and Thrombolysis in Myocardial Infarction (TIMI) grade 0 or 1 flow in the left anterior descending artery underwent coronary ultrasound thrombolysis. Angiographic follow-up was performed after 10 minutes and 12 to 24 hours. Ultrasound induced successful reperfusion (TIMI grade 3 flow) in 87% of the patients. Adjunct percutaneous transluminal coronary angioplasty (PTCA) after ultrasound thrombolysis produced a final residual stenosis of 20 +/- 12% as determined by quantitative coronary angiographic analysis. There were no adverse angiographic signs or clinical effects during the procedure. There was no change in the degree of flow in any of the patients at the 12- to 24-hour angiograms. During hospitalization, 1 patient had recurrent ischemia on the fifth day after the procedure, and emergent catheterization revealed occlusion at the treatment site. The patient was successfully treated with PTCA., Conclusions: These results suggest that ultrasound thrombolysis has the potential to be a safe and effective catheter-based therapeutic modality in reperfusion therapy for patients with AMI and other clinical conditions associated with intracoronary thrombosis.

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.

Objectives: To assess time-consuming procedures in the prehospital stage of acute myocardial infarction patients who had received thrombolytic therapy at the scene, and to evaluate their effect on the clinical outcome., Design: Prospective study., Setting: Mobile intensive care unit staffed by an intern or a hospital-based physician. PARTICIPANTS AND INTERVENTIONS. Thrombolytic therapy with recombinant tissue-type plasminogen activator (total dose of 120 mg/6 hrs) was initiated at the scene in 167 patients. Treatment continued during transportation and thereafter in the cardiac care unit. During hospitalization, radionuclide ventriculograms and coronary angiography were performed in most patients., Measurements and Main Results: Correct diagnosis was confirmed in 165 of 167 patients. Mean time to treatment was 96 +/- 42 (SD) mins with no significant difference between patients treated at home (n = 105) or in public places (n = 60). Global duration of treatment was significantly shorter when thrombolytic therapy was given in public as compared with treatment applied at home (50 +/- 13 vs. 57 +/- 16 mins, respectively, p < .002)., Conclusion: If patients and physicians become aware of the potential advantages of prompt initiation of thrombolytic therapy at the scene, critical time may be saved in delivering thrombolysis to the clotted coronary artery.

Background: The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both., Methods and Results: We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase., Conclusions: The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.

Echocardiographically recorded mitral valve motion was compared with phasic transmitral flow in 17 open chest dogs. The normal mitral valve opening started with the onset of mitral flow and reached its full excursion while flow was still accelerating. Complete valve opening occurred .044 sec (plus or minus .002 sem) before peak flow, during which time an average of 17.6 percent of total mitral filling volume had passed through the valve. In contrast to the opening movement, the closing motion of the anterior mitral valve cusp lagged behind the deceleration of mitral flow. The E-F phase of the mitral valve echogram started while mitral flow was still increasing and resulted from a combined posterior motion of the cusp and the ring. The E-F slope of the normal valve was found to decrease with reduced cardiac output. The amplitude of the anterior cusp excursion did not reflect the amount of mitral flow. Prolonged P-R interval may induce a mid-diastolic reversal of mitral flow which, in turn, may be accompanied by partial or complete valve closure, occurring before the onset of ventricular contraction. Such premature closure of the mitral valve may be accompanied by a certain amount of regurgitant flow.

The aortic valve echogram was recorded in open chest dogs simultaneously with aortic flow, acceleration of flow, aortic and left ventricular pressures, and intracardiac phonocardiograms. Comparison of echographic with hemodynamic data showed the following: The aortic valve started its opening with the onset of flow, at the same point that left ventricular pressure exceeded aortic pressure. Complete valve opening preceded peak aortic flow by an average of 43 msec and the cusps started to move toward closure while flow was still accelerating. Final closure of the valve was achieved at the time of zero flow and preceded the aortic second sound by 4-10 msec. The echographically determined "valve orifice area" correlated well with aortic stroke volume (r = 0.94). The intensity of the aortic first sound was related to peak acceleration of aortic flow. The intensity of the second sound was not related to the amplitude of cusp motion but correlated well with the aortic pressure at the time of closure and with peak flow deceleration.

Ventricular fibrillation in patients without recognizable heart disease is uncommon and electrophysiologic data on such patients is limited. Over a 7 year period, five patients (three men and two women, ranging in age from 24 to 52 years) without demonstrable heart disease underwent electrophysiologic studies with pharmacologic drug testing because of single (four patients) or multiple (one patient) documented episodes of ventricular fibrillation. The arrhythmic event was unrelated to myocardial ischemia or infarction, metabolic or electrolyte disturbances, drug toxicity, preexcitation, or prolonged QT syndromes. In all three patients receiving no antiarrhythmic drugs and in two pretreated with amiodarone, a rapid poorly tolerated ventricular tachyarrhythmia requiring cardioversion was induced by programmed ventricular stimulation with up to two extrastimuli. In all instances, addition of either oral quinidine or oral disopyramide prevented the induction of sustained ventricular arrhythmias. All five patients were placed on antiarrhythmic drug regimens found effective during electrophysiologic studies and remained asymptomatic during follow-up periods ranging from 12 to 93 (mean 52) months. We conclude that in the patients with idiopathic ventricular fibrillation in our study: programmed ventricular stimulation reliably replicated the spontaneous arrhythmia, class I antiarrhythmic agents effectively prevented induction of the arrhythmia in the laboratory, and in contrast to the severity of the presenting arrhythmia, a benign clinical course was observed during long-term therapy with class I antiarrhythmic agents.

Over a 3 year period we evaluated 23 patients (16 men, seven women) with apical hypertrophic cardiomyopathy by noninvasive and invasive methods. Sixteen patients had chest pain. In 17, results of cardiovascular examination were normal. The electrocardiogram showed precordial inverted T waves in all patients and these were of mild-to-moderate amplitude (less than 10 mm) in 18 and giant (greater than 10 mm) in five. M mode echocardiography revealed a typical pattern of contraction and relaxation in the apical region of the left ventricle that was associated with significant hypertrophy. These findings were confirmed by two-dimensional echocardiography. Systolic anterior motion of the mitral valve was not observed nor was there any evidence of obstruction of the left ventricular outflow tract. Results of Doppler echocardiographic study of the mitral and aortic flow were normal in all patients but one who had mild mitral insufficiency. Radionuclide studies of 14 patients revealed a mean left ventricular ejection fraction of 66 +/- 6% (range 55% to 79%), with normal left ventricular contraction in all patients but two with apical hypokinesis. In all six patients who underwent catheterization a characteristic appearance of the left ventricle at end-systole as well as abnormal end-diastolic contour were noted on the left ventricular angiogram, but the "ace of spades" configuration was seen in only one. We conclude that the 23 patients studied form a homogeneous group of individuals with nonobstructive apical hypertrophic cardiomyopathy, which differs in many respects from cardiomyopathies reported by other investigators.

The very high-frequency content (150 to 250 Hz) of epicardial electrogram waveforms was studied in 19 anesthetized dogs subjected to occlusion of left anterior descending coronary artery. Computer techniques of digital averaging and digital band-pass filtering were applied. Signals were obtained from epicardial electrodes placed in the ischemic left ventricular region and on the noninjured right ventricular surface, and from the body surface electrocardiogram. All recordings were made simultaneously before, during, and after coronary occlusion and subjected to the same analysis. The waveforms obtained from the ischemic left ventricular region showed a considerable decrease in high-frequency content, while those obtained from the noninjured right ventricular surface remained unchanged. The results correlated with the appearance of a zone of reduced amplitude in the body surface high-frequency QRS complex. Therefore, this macroscopic phenomenon measured noninvasively from the body surface is explained by local reduction of high-frequency activity in the ischemic region of the myocardium.

We studied the dynamic changes in mitral flow patterns and in mitral valve motion before and after producing acute, reversible aortic insufficiency (AI) in nine open-chest dogs. Phasic mitral flow, the mitral valve echocardiogram, and intracardiac phonocardiogram and other hemodynamic variables were measured. During moderate AI (mean regurgitant fraction 52 +/- 5%) (+/- SD), the antegrade filling volume decreased from 31 +/- 7 to 24 +/- 6 ml (p less than 0.01), but the peak protodiastolic mitral flow rate increased from 139 +/- 37 to 157 +/- 42 ml/sec (p less than 0.01), reflecting the shift of a larger fraction of total mitral filling volume to early diastole. In six dogs, atrial pacing was used to examine the hemodynamic effects of tachycardia. Increasing the heart rate from 90 to 120 beats/min increased cardiac output from 2.64 +/- 0.56 to 3.3 +/- 0.831/min (p less than 0.05) and decreased left atrial pressure from 24 +/- 8 to 17 +/- 7 mm Hg (p less than 0.05). Increasing heart rate to 150 beats/min compromised mitral filling, reduced cardiac output and increased left atrial pressure. Moderate tachycardia improves cardiac performance in AI by reducing regurgitant volume, without significantly reducing transmitral filling volume. The mitral valve echocardiogram showed only a small decrease in cusp opening amplitude during AI. A low-pitched left ventricular inflow tract murmur was recorded in protodiastole and corresponded in time to the rapidly increasing mitral flow. We conclude that the major determinant of the turbulence responsible for the creation of the austin flint murmur is the antegrade mitral flow stream and its mixing with the retrograde aortic flow.

A fetal tachyarrhythmia was discovered at the thirty-second week of gestation of a 22-year old woman. Fetal echocardiography revealed atrial fibrillation with rapid ventricular rate, without any other demonstrable cardiac abnormality. In spite of therapeutic maternal blood levels of digoxin, the fetal ventricular rate and cardiac size increased, which prompted us to perform cesarean section at the thirty-fourth week of gestation. A baby with a Wolff-Parkinson-White syndrome but no other cardiac anomaly was delivered. Recurrent episodes of nonsustained atrial fibrillation with conduction over the accessory pathway occurred in the first hours of life. The Wolff-Parkinson-White pattern was not present on subsequent ECG recordings. The use of echocardiography in the diagnosis and management of this rare fetal tachyarrhythmia is emphasized.

We studied the physiology of pulmonary venous flow in 13 normal subjects and five patients with atrial rhythm disorders and atrioventricular conduction disturbances with pulsed Doppler and two-dimensional echocardiography. The left atrium, mitral valve, and pulmonary venous ostia were visualized through the apical four-chamber view. Mitral and pulmonary venous flows were obtained by placing the Doppler sample volume at the appropriate orifice. Pulmonary venous flow was biphasic: a rapid filling wave was observed during systole when the mitral valve was closed; a second wave was observed in diastole during the rapid ventricular filling phase of mitral flow, but was significantly delayed. In patients without atrial contraction (atrial fibrillation and sinoatrial standstill), the initial rapid filling was greatly diminished and only the second diastolic wave appeared to contribute to left atrial filling. In patients with high-grade atrioventricular block, each atrial contraction was followed by a surge in flow from the pulmonary veins. These results are consistent with data obtained from invasive measurements in both dogs and man, and confirm the validity of the use of pulsed Doppler echocardiography in the study of pulmonary venous flow. We suggest that pulmonary venous flow is influenced by dynamic changes in left atrial pressure created by contraction and relaxation of the atrium and ventricle. The initial peak in pulmonary venous flow occurs with atrial relaxation simultaneously with the reduction of left atrial pressure, and the second peak occurs with left ventricular relaxation and rapid transmitral filling of the ventricle.

The efficacy, electrophysiologic effects, and side effects of adenosine triphosphate (ATP) and verapamil in the short-term management of paroxysmal reciprocating junctional tachycardia (PRJT) were compared in 20 patients. All patients had inducible sustained PRJT during control electrophysiologic study. Fourteen patients had PRJT involving a retrograde accessory pathway, and six patients had atrioventricular (AV) nodal reentrant tachycardia ("slow-fast" type). ATP, which has a very short half-life, was first administered (10 mg iv over 1 sec) during sustained PRJT. If PRJT did not terminate within 2 min, a bolus of 20 mg ATP was given. Verapamil (5 mg iv over 15 sec) was subsequently administered during sustained PRJT, and if the latter did not terminate within 3 min another bolus of 5 mg verapamil was given. The cycle lengths of PRJT before administration of 10 or 20 mg ATP and 5 mg verapamil were similar. The 10 mg dose of ATP terminated PRJT in 17 of the 20 patients, and 20 mg ATP was required to terminate PRJT in the three remaining patients. The 5 mg dose of verapamil terminated PRJT in 15 patients, whereas an additional bolus of 5 mg terminated PRJT in one of the remaining five patients. The overall efficacy of ATP (20/20, 100%) was significantly greater than that of verapamil (16/20, 80%) (p less than .05); however, there was no significant difference between the conversion rate of PRJT after administration of 10 mg ATP (17/20) and 5 mg verapamil (15/20). ATP terminated PRJT more quickly than verapamil (mean 24 sec vs mean 51 sec; p less than .01). Termination of PRJT by either ATP or verapamil was mainly related to a block in the AV node in patients with accessory pathways and to a block in the antegrade slow pathway in patients with AV nodal reentry. Cycle length alternans before termination of tachycardia was observed more frequently after verapamil than after ATP (7/16 vs 1/20; p less than .01). The total incidence of transient second-degree AV nodal block and various cardiac supraventricular and ventricular arrhythmias was higher after termination of PRJT by ATP than after verapamil (17/20 vs 5/16; p less than .001). A higher incidence of transient but frequently uncomfortable noncardiac side effects was observed after ATP. We conclude that ATP (10 to 20 mg) is more effective and more rapid than verapamil (5 or 5 + 5 mg) in terminating PRJT but results in a higher incidence of cardiac and noncardiac side effects.(ABSTRACT TRUNCATED AT 400 WORDS)

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.