Effect of inotropic stimulation on motion and thickening of the ventricular septum following either coronary artery bypass grafting or mitral valve replacement for mitral stenosis.
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Biomedical subjects
Publications and source records attributed to E Kaplinsky.
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The diagnosis of acute coronary syndromes is frequently missed, and many high-risk patients fail to be admitted to hospital. The aim of this study was to assess the value of cardiac markers in ruling out acute ischemic events in patients with symptoms of possible cardiac origin and nondiagnostic electrocardiograms. The data collected between May 1999 and April 2000 for this prospective cohort study were retrieved from the records of 777 consecutive prehospital patients (mean age 70 years, 62.9% men) whose symptoms lasted for 6 to 48 hours, who were treated by mobile intensive care teams, and for whom the physician could not reach a clear-cut decision whether they should be taken to hospital or left at home. The cardiac markers, creatine kinase (CK-MB), myoglobin, and troponin I, were measured at the scene using a rapid Stat kit to qualitatively detect their presence in whole blood samples. Results were determined after 15 minutes at the scene. The assay was positive in 30 patients, 11 of whom had a definite cardiac diagnosis (acute myocardial infarction in 4 and unstable angina pectoris in 7). Positive and negative predictive values of the assay for detecting a significant coronary event were 36.7% and 100%, respectively. Of the 747 patients with a negative result, 6 patients had a false result (1 with myocardial infarction and in 5 with unstable angina) (99.2% negative predictive value). Thus, cardiac markers are useful in ruling out high-risk coronary syndromes in the prehospital setting when the clinical presentation and electrocardiogram are inconclusive.
BACKGROUND: Acute myocardial infarction (AMI) associated with significant left ventricular dysfunction (LVD) indicates a poor prognosis. Previous studies suggested that revascularization improves survival of patients with AMI complicated by cardiogenic shock. However, other studies that suggested that revascularization improves survival of stable patients with significant LVD did not specifically address patients who had recently had an AMI. OBJECTIVES: Our purpose was to determine whether patients with thrombolysis-treated AMI associated with significant LVD are likely to incur a survival advantage from catheterization and coronary revascularization performed within 30 days after AMI. METHODS: The study population was drawn from the Argatroban in Acute Myocardial Infarction-2 (ARGAMI-2) trial, which included 1200 patients with AMI, all of whom received thrombolytic therapy. Our analysis included 737 patients for whom LV function was estimated by echocardiography. Two hundred two patients had significant LVD; of them, 117 (58%) underwent cardiac catheterization and 85 were treated noninvasively. Among 535 patients without significant LVD, 291 (54%) underwent cardiac catheterization and 244 were treated noninvasively. RESULTS: Compared with a noninvasive approach, an invasive approach resulted in reduced 30-day and 6-month mortality rates in patients with significant LVD: 4.3% versus 10.6%, adjusted odds ratio (OR) 0.26, 95% confidence interval (CI) 0.04 to 1.18, and 6.1% versus 15.5%, OR 0.27, 95% CI 0.06 to 0.98, respectively. A similar comparison in patients without significant LVD resulted in comparable 30-day and 6-month mortality rates for both patient groups: invasively versus noninvasively treated, 0.7% versus 0.8%, OR 1.04, 95% CI 0.04 to 12.7, and 1.4% versus 1.7%, adjusted OR 1.60, 95% CI 0.20 to 9.87. CONCLUSIONS: The current study suggests that AMI patients with significant LVD may benefit from cardiac catheterization and revascularization performed early after AMI, whereas in patients without significant LVD the outcome of those treated invasively or conservatively was similar.
BACKGROUND: Patients with recurrent acute myocardial infarction (AMI) are at increased risk for morbidity and mortality. We compared the outcome of patients with recurrent AMI hospitalized in coronary care units in the prereperfusion and reperfusion eras. METHODS: The study population comprised 2 large-scale cohorts with recurrent AMI: (1) 1415 (24%) of 5839 consecutive patients with AMI hospitalized in 1981 to 1983 (Secondary Prevention Reinfarction Israeli Nifedipine Trial [SPRINT] Registry) and (2) 1093 (25%) of 4317 patients with AMI from three national surveys performed in 1992 to 1996. RESULTS: Patients in the 1990s had significantly lower rates of heart failure and cardiogenic shock. The 7-day mortality declined from 18% in 1981-1983 to 10% in 1992-1996 (adjusted odds ratio [OR] 0.57 [0.44-0.75]), the 30-day mortality rate from 26% to 16% (OR 0.56 [0.44-0.71]), and the 1-year mortality rate from 39% to 26% (adjusted hazard ratio [HR] 0.64 [0.54-0.75]), respectively. In the 1992-1996 cohort, the adjusted risk of 7-day, 30-day, and 1-year mortality for patients with recurrent AMI treated with thrombolysis in comparison to patients without thrombolysis was OR 1.69 (1.07-2.65), 1.52 (1.03-2.23), and HR 1.18 (0.90-1.55), respectively. The mortality rate among patients treated with early percutaneous transluminal coronary angioplasty/coronary artery bypass grafting was 3% versus 12% at 7 days (OR 0.36 [0.16-0.73]), 7% versus 18% at 30 days (OR 0.45 [0.25-0.77]), and 16% versus 29% at 1 year (HR 0.64 [0.46-0.96]), in comparison to patients without revascularization. CONCLUSION: The prognosis of patients with recurrent AMI improved significantly during the reperfusion era. Although thrombolysis may have a limited therapeutic effect among patients with recurrent AMI, an interventional approach seems more appropriate when indicated. A randomized trial of thrombolysis versus early revascularization is needed in patients with recurrent AMI.
A 19-year-old man with a previous diagnosis of Borjeson-Forssman-Lehmann syndrome was referred for heart transplantation after a dilated cardiomyopathy was found. This is the first known report of Borjeson-Forssman-Lehmann syndrome and dilated cardiomyopathy; possible explanations for this infrequent association are revised. The purpose of the present report is to highlight the importance of cardiovascular investigation in this syndrome.
Following transvenous implantable cardioverter defibrillator shocks, a significant increase in QT dispersion was observed. We suggest shock-induced increased dispersion of myocardial repolarization as one of the mechanisms of shock-induced proarrhythmia.
BACKGROUND: The decay of the pressure gradient across a stenotic mitral valve is determined by the size of the orifice and net AV compliance (C(n)). We have observed a group of symptomatic patients, usually in sinus rhythm, characterized by pulmonary hypertension (particularly during exercise) despite a relatively large mitral valve area by pressure half-time. We speculated that this discrepancy was due to low atrial compliance causing both pulmonary hypertension and a steep decay of the transmitral pressure gradient despite significant stenosis. We therefore tested the hypothesis that C(n) is an important physiological determinant of pulmonary artery pressure at rest and during exercise in mitral stenosis. METHODS AND RESULTS: Twenty patients with mitral stenosis were examined by Doppler echocardiography. C(n), calculated from the ratio of effective mitral valve area (continuity equation) and the E-wave downslope, ranged from 1.7 to 8.1 mL/mm Hg. Systolic pulmonary artery pressure (PAP) increased from 43+/-12 mm Hg at rest to 71+/-23 mm Hg (range, 40 to 110 mm Hg) during exercise. There was a particularly close correlation between C(n) and exercise PAP (r=-0.85). Patients with a low compliance were more symptomatic (P<0.025). Catheter- and Doppler-derived values for C(n), determined in 10 cases, correlated well (r=0.79). CONCLUSIONS: C(n), which can be noninvasively assessed, is an important physiological determinant of PAP in mitral stenosis. Patients with low C(n) represent an important clinical entity, with symptoms corresponding to severe increases in PAP during stress echocardiography.
Impaired relaxation is frequently masked by elevated filling pressures, resulting in a pseudonormal flow pattern (E/A >1.0). Because the E/A wave ratio increases as filling pressures rise, it is generally assumed that patients with an E/A ratio of <1.0 (impaired relaxation pattern) have relatively low filling pressures. Nevertheless, patients with an E/A ratio of <1.0 can have as profoundly elevated filling pressures as patients with a pseudonormal or restrictive filling pattern. Because left ventricular (LV) pressure during end-diastole essentially determines atrial afterload, the response of the A-wave velocity to a reduction of atrial afterload by a standardized Valsalva maneuver should allow estimation of LV end-diastolic pressure (LVEDP) regardless of the baseline Doppler flow pattern. This was tested in 20 consecutive patients who were studied by pulse-wave Doppler echocardiography during cardiac catheterization. There was a close correlation between LVEDP and the change in A-wave velocity during the Valsalva maneuver (r = 0.85, SEE 6.7 mm Hg) regardless of the baseline E/A ratio. In patients with a LVEDP of <15 mm Hg the A wave decreased by 21 +/- 15 cm/s. In patients with a LVEDP of >25 mm Hg the A wave increased by 18 +/- 13 cm/s. The change in the E/A ratio during Valsalva correlated fairly with LVEDP (r = -0.72, SEE 8.8 mm Hg), the baseline E/A ratio correlated poorly, and scatter was substantial (r = 0.46, SEE 11.2 mm Hg). Just as elevated filling pressures can mask impaired relaxation, the impaired relaxation pattern can mask the presence of elevated filling pressures. This can be revealed by testing the response of the A wave to the Valsalva maneuver, allowing estimation of LVEDP independent of the baseline E/A ratio.
BACKGROUND: The rising cost of services provided by hospital emergency departments is of major concern. Attempts to reduce the costs of emergency cardiac care have thus far focused primarily on medical and administrative management in the hospital. The role of the patient in appropriate prehospital decision-making has been generally ignored. HYPOTHESIS: Membership in "Shahal" (an integrative telemedicine system) may have beneficial effects on patient decision-making and national health costs. METHODS: During a 6-month period, a random group of subscribers who had called for medical assistance during the previous 24 h were asked what action they would have taken had they not been Shahal subscribers. All study patients were followed for at least 7 days. RESULTS: In all, 1,608 subscribers (age 71 +/- 13 years) were included. Of these, 514 replied that they "would have waited," 363 "would have contacted their physicians," and 731 "would have sought emergency department care." Of the presenting medical problems, 86% were resolved without utilizing hospital facilities. A mobile intensive care unit was dispatched in 412 (26%) cases. A cost estimate of abuse indicated that the service resulted in a savings to the national economy of approximately $830,000 per 10,000 members per year. CONCLUSIONS: This study demonstrated that Shahal membership can reduce costs of medical care and the number of hospital emergency department visits.
The individual activities of sodium versus calcium channels in the initiation and maintenance of ventricular fibrillation (VF) have not been fully elucidated. Therefore we studied in isolated heart under nonischemic conditions (a) VF characteristics in untreated hearts, (b) initiation and maintenance of VF during attenuation and blockade of slow calcium channel activity by verapamil, (c) the effect of these interventions on the characteristics of the induced arrhythmia, and (d) the impact of heart weight on the observed results. Measurements were carried out in both ventricles of isolated feline hearts during ventricular pacing and 8 min of electrically induced tachyarrhythmias. Measurements during ventricular pacing included epicardial conduction time (CON), refractoriness (VRP), and all tissue resistivity (ATR; an indirect measure of changes in intercellular electrical coupling). Measurements during arrhythmia included ATR, peak frequency [PKF; a measure of the prevailing frequency based on Fast Fourier Transform (FFT) analysis], and normalized entropy (ENTROP; a measure of the degree of arrhythmia organization). Measurements during sinus rhythm and arrhythmia were repeated after blocking of calcium channel activity by verapamil at a high concentration (1.8x10(-4) M; n = 8) and at two low concentrations (1.5 and 3.0x10(-7) M; n = 8). In untreated hearts, mainly VF episodes were induced, exhibiting a low degree of organization with no significant change in this parameter throughout the arrhythmia (8 min). In the left ventricle (LV; and to a much smaller extent in the right ventricle; RV), a gradual increase in PKF was observed throughout the arrhythmia, with no significant change in ATR. Verapamil at a high concentration increased CON, but did not affect VRP. These findings were similar in both ventricles. In lower verapamil concentrations, CON was not affected, and VRP was slightly shortened. After treatment with a high verapamil concentration, VF could not be induced in small hearts but was always inducible in large hearts. Transient arrhythmia episodes appeared in 9% of untreated hearts, in 25% with "high" verapamil, and in 25-37% with "low" verapamil. With all verapamil concentrations, the induced arrhythmia was modulated from a predominantly VF to PVT or MVT type, manifested by a decrease in ENTROP. This effect was less pronounced with increasing heart weight. No significant change in PKF and in ATR was obtained with verapamil throughout the arrhythmia. It is suggested that verapamil modulation of arrhythmia organization is associated mainly with a direct blockade of calcium channel activity (perhaps by causing reduction in the safety factor for conduction), rather than with indirect modulation of electrophysiological parameters.
Because the role of sodium channels in the initiation and maintenance of VF is not fully elucidated, we studied the significance of sodium channel activity in VF using sodium channel blockers. In nonischemic isolated feline hearts, the following electrophysiologic parameters were measured before and after application of tetrodotoxin (5 x 10(-7) M, n = 6) or lidocaine (1 x 10(-5) M, n = 8): (a) during pacing, epicardial conduction time; refractoriness; the fastest rate for 1:1 pacing/response capture, and all tissue resistivity, indirectly reflecting intercellular electrical resistance; (b) during 8 min of electrically induced tachyarrhythmias, all tissue resistivity; peak frequency (to measure average frequency based on fast-Fourier transformation analysis); and normalized entropy (to measure the degree of arrhythmia organization). In nonischemic isolated rabbit hearts (n = 4), three-dimensional mapping was performed before and after application of lidocaine (1 x 10(-5) M). In feline hearts, lidocaine and tetrodotoxin application resulted in: (a) more spontaneous arrhythmia termination (63-67%) than in nontreated hearts (7%); (b) transformation from mainly VF into ventricular tachycardia with increased organization; and (c) prolongation of conduction time (155-248%) (p < 0.01 for all parameters). The ventricular refractory period was slightly prolonged by tetrodotoxin in the right ventricle and exhibited rate-dependent shortening in control and with lidocaine. Tetrodotoxin and lidocaine reduced the pacing rate for 1:1 pacing/response capture, and all tissue resistivity was not significantly affected. Peak frequency was decreased by tetrodotoxin and lidocaine mainly in the left ventricle (p < 0.01). In nontreated left ventricles, peak frequency was increased over time but was attenuated by lidocaine. In isolated rabbit hearts, several simultaneous wave fronts were detected during VF in nontreated hearts and were reduced to only one or two major wavefronts after application of lidocaine. Suppression of sodium channel activity that primarily slowed conduction time and had little or no effect on ventricular refractory period and all tissue resistivity resulted in less stable and more organized arrhythmias and reduced tachyarrhythmia rate compared with nontreated hearts. These results suggest an active role for sodium channels in the maintenance of ventricular fibrillation.
BACKGROUND: Left-ventricular pseudohypertrophy reflecting left-ventricular compression was reported in a selected group of patients with cardiac tamponade. HYPOTHESIS: Criteria for the presence of pseudohypertrophy can be established to guide its use as a sign of left-ventricular compression in patients with cardiac tamponade. METHODS: Left-ventricular wall thickness, diameters, relative diastolic wall thickness (%) = (posterior wall thickness/end diastolic radius) x 100 and estimated left-ventricular mass were measured in patients with small, moderate and large pericardial effusion, in patients with cardiac tamponade before and after pericardiocentesis (16 patients in each group) and in 30 control subjects with normal echocardiograms. RESULTS: Left-ventricular posterior wall thickness was increased (12 +/- 2 vs. 9 +/- 1 mm, p < 0.001), left-ventricular end-diastolic diameter was reduced (3.9 +/- 0.5 vs. 4.6 +/- 0.3 cm, p < 0.001) and relative left-ventricular diastolic wall thickness was increased (61 +/- 13 vs. 41 +/- 4.5%, p < 0.001) only in patients with cardiac tamponade compared to controls, but not in patients with small, moderate and large effusions, respectively (relative wall thickness: 42 +/- 5, 41 +/- 7 and 44 +/- 7%, p = NS). Mean values of the estimated left-ventricular mass were similar in all groups. Following pericardiocentesis all parameters were normal. CONCLUSIONS: Despite normal left-ventricular mass, relative left-ventricular diastolic wall thickness is elevated in patients with cardiac tamponade. In contrast it is normal in patients with various degrees of pericardial effusion supporting its use as a quantitative measure of left-ventricular compression in patients with suspected cardiac tamponade.
OBJECTIVE: To study the importance of a J shape in atrial pacing leads. PATIENTS AND METHODS: We compared in a randomized controlled study acute and chronic results with 2 steroid-eluting, polyurethane, screw-in atrial lead models that differ only in shape. A total of 208 patients were randomized to have implantation of either a straight atrial lead (n = 105) or a J-shaped atrial lead (n = 103). Patients were followed up for 1 year. RESULTS: On implantation, there were no significant differences between leads in rates of failure to implant, implant measurements, number of attempts to achieve an acceptable position, and fluoroscopy times. Before discharge and at 3-month and 1-year follow-up, electrical measurements showed no statistical differences between leads. During the first year after implantation, there were 2.9% early dislodgments (< 1 week after implantation) and 2.9% late dislodgments in the straight lead group (5.9% rate of all dislodgments) vs no dislodgments in the J-shaped lead group (P = .01). There was a trend toward higher rates of exit block and lead malfunction in the J-shaped lead group. Rates of pericardial complications, subclavian/axillary thrombosis, and chronic atrial fibrillation were the same in both groups. CONCLUSIONS: Both leads appear to have an equally favorable performance profile for 1 year of follow-up. The J-shaped lead seems to be more stable and have fewer dislodgments, although it may have a somewhat higher malfunction rate.
No "white coat" effect contaminated the validity of measurements in 30 participants in a "Telepress" program, in which subscribers to a telecardiologic facility transtelephonically transmit their self-measured blood pressure values.
OBJECTIVES: This study was done to determine whether electrocardiographic (ECG) isolated ST-segment elevation (ST) in posterior chest leads can establish the diagnosis of acute posterior infarction in patients with ischemic chest pain and to describe the clinical and echocardiographic characteristics of these patients. BACKGROUND: The absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis of these infarcts and thus may result in inadequate triage and treatment. Although 4% of all acute myocardial infarction (AMI) patients reveal the presence of isolated ST in posterior chest leads, the significance of this finding has not yet been determined. METHODS: We studied 33 consecutive patients with ischemic chest pain suggestive of AMI without ST in the standard ECG who had isolated ST in posterior chest leads V7 through V9. All patients had echocardiographic imaging within 48 h of admission, and 20 patients underwent coronary angiography. RESULTS: Acute myocardial infarction was confirmed enzymatically in all patients and on discharge ECG pathologic Q-waves appeared in leads V7 through V9 in 75% of the patients. On echocardiography, posterior wall-motion abnormality was visible in 97% of the patients, and 69% had evidence of mitral regurgitation (MR), which was moderate or severe in one-third of the patients. Four patients (12%), all with significant MR, had heart failure, and one died from free-wall rupture. The circumflex coronary artery was the infarct related artery in all catheterized patients. CONCLUSIONS: Isolated ST in leads V7 through V9 identify patients with acute posterior wall myocardial infarction. Early identification of those patients is important for adequate triage and treatment of patients with ischemic chest pain without ST on standard 12-lead ECG.
OBJECTIVES: To determine the prevalence and clinical significance of early ST segment elevation resolution after primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI). BACKGROUND: Despite angiographically successful restoration of coronary flow early during AMI, adequate myocardial reperfusion might not occur in a substantial portion of the jeopardized myocardium due to microvascular damage. This phenomenon comprises the potentially beneficial effect of early recanalization of the infarct related artery (IRA). METHODS: Included in the study were 117 consecutive patients who underwent angiographically successful [Thrombolysis in Myocardial Infarction (TIMI III)] primary PTCA. The patients were classified based on the presence or absence of reduction > or =50% in ST segment elevation in an ECG performed immediately upon return to the intensive cardiac care unit after the PTCA in comparison with ECG before the intervention. RESULTS: Eighty-nine patients (76%) had early ST segment elevation resolution (Group A) and 28 patients (24%) did not (Group B). Group A and B had similar clinical and hemodynamic features before referring to primary PTCA, as well as similar angiographic results. Despite this, ST segment elevation resolution was associated with better predischarge left ventricular ejection fraction (LVEF) (44.7 +/- 8.0 vs. 38.2 +/- 8.5, p < 0.01). Group B patients, as compared with those of Group A, had a higher incidence of in-hospital mortality (11% vs. 2%, p = 0.088), congestive heart failure (CHF) [28% vs. 19%, odds ratio (OR) = 4, 95% confidence interval (CI) 1 to 15, p = 0.04], higher long-term mortality (OR = 7.3, 95% CI 1.9 to 28, p = 0.004 with Cox proportional hazard regression analysis) and long-term CHF rate (OR = 6.5, 95% CI 1.3 to 33, p = 0.016 with logistic regression). CONCLUSIONS: Absence of early ST segment elevation resolution after angiographically successful primary PTCA identifies patients who are less likely to benefit from the early restoration of flow in the IRA, probably because of microvascular damage and subsequently less myocardial salvage.
AIMS: To determine the circadian rhythm of paroxysmal atrial fibrillation in a very large outpatient population. METHODS AND RESULTS: We reviewed all emergency telephone calls received in Shahal (a medical service covering 44 000 subscribers), from 1987 to 1997. Patients were included if new-onset atrial fibrillation was recorded. During this study period, 9989 episodes of paroxysmal atrial fibrillation were recorded. The time of onset was not uniformly distributed throughout the 24 h period. Instead, the distribution of arrhythmic episodes showed a double peak, with a significant increase in the number of episodes in the morning and a second rise in the evening (P<0.001). A non-uniform weekly distribution of events was also noted, with substantially fewer episodes on Saturdays (P<0.001). Finally, more arrhythmias occurred during the last months of each year (P<0.001). CONCLUSIONS: The onset of paroxysmal atrial fibrillation does not occur randomly. The large patient population in the present study suggests that the circadian rhythm of paroxysmal atrial fibrillation is similar to that described for other cardiovascular diseases, with clustering of events in the morning and (to a lesser degree) late in the evening. Weekly and yearly circadian patterns are also prominent.
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.