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PubMed2005

A decrease of enlarged left atrium following cardioversion of atrial fibrillation predicts the long-term maintenance of sinus rhythm.

BACKGROUND: Although increased left atrial size (LA) has been long regarded as one of the factors negatively influencing the long-term maintenance of sinus rhythm (SR) following cardioversion (CV) of atrial fibrillation (AF), some reports suggested that CV might be effective also in patients with large LA.Aim. We sought to determine the role of LA enlargement in long-term SR maintenance after CV of persistent AF. METHODS: 104 consecutive patients (33 females, 71 males, mean age 60.4+/-7.4 years) were assigned to SR restoration and maintenance with serial antiarrhythmic drugs. Transthoracic echocardiographic (TTE) variables were recorded prior to CV. Generalised additive logistic regression was used to investigate the impact of LA enlargement on the long-term SR maintenance. RESULTS: SR was present in 63.5% of patients after one year of follow-up. Increased LA area >28 cm (RR 1.72; 1.09-2.71; p<0.02) and increased fractional shortening values in ranges between 26-40% (1.2; 1.01-1.44; p<0.05) were significantly associated with SR maintenance after one year. In order to determine the influence of the LA diameter on the probability of SR maintenance, we analysed mean LA(ar) values prior to and after CV. Patients with large LA(ar) (28 cm(2)) presented a significant decrease of LA size (31.45+/-3.07 cm(2) vs 28.94+/-3.81 cm(2); p<0.008) during the first 30 days after SR restoration. In the group of patients with LA(ar) 28 cm(2) we noted decrease in LA size by 2.57+/-3.2 cm(2), whereas in patients with a smaller LA volume this decrease was significantly lower, being 0.47+/-2.9 cm(2) (p<0.004). CONCLUSIONS: LA enlargement does not preclude a favourable outcome after CV of AF. The decrease in LA area occurring during 30 days following CV favours long term SR maintenance.

Aged↗
PubMed1995

Determination of left ventricular chamber stiffness from the time for deceleration of early left ventricular filling.

BACKGROUND: A noninvasive measure of left ventricular (LV) chamber stiffness (KLV) would be clinically useful. Our theoretical analysis predicts that KLV can be calculated from the time for deceleration of LV early filling (tdec) by [formula: see text] where p = density of blood, L = effective mitral length, and A = mitral area. METHODS AND RESULTS: We tested this hypothesis in eight conscious dogs instrumented for measurement of LV pressure (P) with use of a micromanometer and volume (V) with use of sonomicrometers. KLV was determined as the slope of the late diastolic portion of the LV P-V loop. KLV was varied from 0.99 +/- 0.35 to 2.58 +/- 0.92 mm Hg/mL with use of three graded doses of phenylephrine. We assumed that p = 1.0 and that L/A = 3.4. Thus, we predicted that KLV = (0.08/tdec)2. The LV filling pattern was determined from the derivative of LV volume (dV/dt). tdec was measured from peak early filling to the end of early filling. Predicted KLV and actual KLV were closely correlated (r = .94, SEE = 0.06 mm Hg/mL, P < .05). The regression line was close to the line of identity (slope = 0.95, intercept = 0.13 mm Hg/mL). Dobutamine did not alter the relation between tdec and KLV.tdec determined from the mitral valve flow velocity measured with Doppler echocardiography correlated well with that measured by dV/dt (r = .89, P < .01) but was 0.02 seconds longer. KLV-calculated tdec from the corrected Doppler tdec provided a good estimate of measured KLV (r = .75, SEE = 0.5 mm Hg/mL, P < .01). CONCLUSIONS: LV chamber stiffness can be determined from the time for deceleration of LV early filling, which can be measured noninvasively.

Animals↗
PubMed2002

Significance of anterior Q waves in left anterior fascicular block--a clinical and noninvasive assessment.

BACKGROUND: Electrocardiographic (ECG) Q waves in V leads (V2 or V3) pose a diagnostic challenge in the presence of left anterior fascicular block (LAFB). Benign Q waves in the absence of coronary artery disease (CAD) primarily due to LAFB have been described. This study evaluates Q waves in the presence of LAFB. HYPOTHESIS: Anterior Q waves in the presence of LAFB may not be indicative of myocardial infarction (MI). METHODS: From 1990 to 1997, ECGs of 236 male patients with LAFB were analyzes for presence of Q waves in the V leads. Records were reviewed for evidence of CAD. Of 236 patients with LAFB, 61 (26%) had Q waves in the V leads. In this group, 31 patients were available for further analysis. RESULTS: Of the 31 patients with Q waves in the V leads who were available for further study, LAFB was present in 22 patients (71%) and LAFB plus right bundle-branch block (RBBB) were present in 9 (29%). Of 20 patients with Q waves due to MI, 13 (65%) had LAFB and 7 (35%) had LAFB plus RBBB. Of 11 patients with benign Q waves, 9 (82%) and 2 (18%) had LAFB and LAFB plus RBBB, respectively. Benign Q waves were noted in 5.3% (11/206) patients with LAFB. The mean duration of Q waves and Q-wave location limited to V2 and/or V3 are 0.029 s and 64% versus 0.053 s and 15% in benign versus pathologic Q waves, respectively. CONCLUSION: Patients with LAFB in the absence of MI may have Q waves in the V leads that are approximately 0.02 s in duration and restricted to one or two leads. This anomaly may represent a variation of conduction in the initial 0.02 s QRS vector due to LAFB.

Adult↗
PubMed1997

L-arginine prevents cyclosporin A-induced pulmonary vascular dysfunction.

BACKGROUND: Cyclosporin A is known to alter endothelium-dependent responses to different agonists. Few data are available concerning the effect of cyclosporin A on the pulmonary vascular bed. METHODS: The endothelium-dependent responses to acetylcholine (20 micrograms), bradykinin (5 micrograms), and substance P (5 micrograms) were investigated in a dog model of left lung autoperfusion at constant flow. RESULTS: The vasodilator response to bradykinin and substance P was significantly decreased with cyclosporin A (20 mg) administration. The average decreases in pulmonary arterial pressure with bradykinin were 5.4 +/- 1.5 mm Hg and 2.4 +/- 0.4 mm Hg before and after cyclosporin A administration, respectively (p = 0.04). The average decreases in pulmonary arterial pressure with substance P were 4.4 +/- 1.0 mm Hg and 1.8 +/- 0.5 mm Hg before and after cyclosporin A administration, respectively (p = 0.04). The responses to acetylcholine and the endothelium-independent relaxing agent nitroglycerin were not significantly affected by cyclosporin A. The effects of cyclosporin A on endothelium-dependent responses to bradykinin and substance P were overcome by the administration of L-arginine (200 mg/kg intravenously). The decreased response to bradykinin and substance P after cyclosporin A administration was not significantly affected by indomethacin, a cyclooxygenase inhibitor. The pulmonary angiotensin-converting enzyme activity was also measured using [3H]benzoyl-phenylalanyl-glycyl-proline, an inactive angiotensin-converting enzyme substrate. There was an average [3H]benzoyl-phenylalanyl-glycyl-proline hydrolysis of 54% +/- 2% and 55% +/- 2% before and after cyclosporin A administration, respectively (not significant). CONCLUSIONS: The present study suggests that cyclosporin A selectively decreases endothelium-dependent responses to bradykinin and substance P without affecting the cyclic guanosine monophosphate-dependent pathway in the canine pulmonary vascular bed. The decreased endothelium-dependent responses to bradykinin and substance P are not related to increased angiotensin-converting enzyme activity. The toxic effect of cyclosporin A on endothelium-dependent responses is reversible by the administration of L-arginine, a source of substrate for nitric oxide.

Acetylcholine↗
PubMed1992

A mathematical model for the quantification of mitral regurgitation. Experimental validation in the canine model using contrast echocardiography.

BACKGROUND: Because the clearance of contrast from the left atrium (LA) relative to the left ventricle (LV) depends on the degree of mitral regurgitation (MR), we hypothesized that a mathematical model can be developed that would provide a quantitative estimation of MR from the washout of contrast from these chambers. METHODS AND RESULTS: After mathematically developing the model, we performed experiments in two groups of dogs with the use of contrast echocardiography. Group 1 consisted of nine dogs in which different degrees of MR were produced by creating ischemic LV dysfunction. Contrast was injected into the LV, and MR was graded visually on a scale of from 0 to 4+. Videointensity plots generated from the LA and LV were provided to the model. There was excellent correlation between visual assessment of MR and model-derived regurgitant fraction in the 33 stages: y = 0.16x + 0.002 (r = 0.97, p less than 0.001, SEE = 0.06). To obtain a more quantitative validation, we placed electromagnetic flow probes on the aorta and just cephalad to the mitral annulus in six dogs (group 2) during cardiopulmonary bypass. Different degrees of MR were produced by chordal traction and/or myocardial ischemia. Regurgitant fraction was calculated at each stage from the flow probe and videointensity data. There was excellent correlation between flow probe and model-derived regurgitant fraction (y = 0.90x + 0.03; r = 0.96, p less than 0.001, SEE = 0.06), and close interobserver and intraobserver correlations were noted using flow probe and contrast echocardiographic data. CONCLUSIONS: A mathematical model that uses the clearance of contrast from the LA relative to the LV can be used to accurately measure the severity of MR. These findings may have important practical implications for the quantification of MR.

Animals↗
PubMed1993

High resolution mapping of Koch's triangle using sixty electrodes in humans with atrioventricular junctional (AV nodal) reentrant tachycardia.

BACKGROUND: Recent evidence suggests that atrioventricular junctional reentrant tachycardia (AVJRT) uses a reentrant circuit that involves the atrioventricular (AV) node, the atrionodal connections, and perinodal atrial tissue. Electrogram morphology has been used to target the delivery of radiofrequency energy to the site of the "slow pathway," a component of this reentrant circuit. The aim of this study was to localize precisely the sites of atrionodal connections involved in AVJRT and to examine atrial electrogram morphologies and their spatial distribution over Koch's triangle. METHODS AND RESULTS: Electrical activation of Koch's triangle and the proximal coronary sinus was examined in 13 patients using a 60-point plaque electrode and computerized mapping system. Recordings were made during sinus rhythm (n = 12), left atrial pacing (n = 8), ventricular pacing (n = 12), and AVJRT (n = 12). During sinus rhythm electrical activation approached Koch's triangle and the AV node from the direction of the anterior limbus, activating the anterior part of the triangle before the posterior part. A zone of slow conduction during sinus rhythm was found within Koch's triangle in 64% of patients. The pattern of atrial activation in Koch's triangle during anterograde fast pathway conduction was similar to that seen during anterograde slow pathway conduction. Retrograde fast pathway conduction during ventricular pacing and during anterior (typical) AVJRT caused earliest atrial activation at the apex of Koch's triangle near the AV node-His bundle junction. In individual patients the site of earliest atrial activation was similar for both anterior AVJRT and retrograde fast pathway conduction during ventricular pacing. Retrograde slow pathway conduction during ventricular pacing and during posterior (uncommon or atypical) AVJRT caused earliest atrial activation posterior to the AV node near the orifice of the coronary sinus. This posterior or "slow pathway" exit site was 15 +/- 4 mm from the His bundle. In individual patients the site of earliest atrial activation was similar for both posterior AVJRT and retrograde slow pathway conduction during ventricular pacing. In one patient anterograde and retrograde conduction occurred via separate slow pathways during AVJRT: Complex atrial electrograms with two or more components were observed near the coronary sinus orifice and in the posterior part of Koch's triangle in all cases. These were categorized as either low or high frequency potentials according to the rapidity of the second component of the electrogram. Low frequency potentials were present at the site of earliest atrial excitation during retrograde slow pathway conduction in 5 of 5 cases (100%) and high frequency potentials in 4 of 5 cases (80%). However, both slow and high frequency potentials could be found at sites up to 16 mm from the site of earliest atrial excitation. CONCLUSIONS: At least two distinct groups of atrionodal connections exist. The site of earliest atrial activation during anterior AVJRT is similar to that of fast pathway conduction during ventricular pacing. This site is close to the His bundle-AV node junction. The site of earliest atrial activation during posterior AVJRT is similar to that of slow pathway conduction during ventricular pacing. This site is near the coronary sinus orifice, approximately 15 mm from the His bundle. The anterograde slow pathway appears to be different from the retrograde slow pathway in some patients. Double atrial electrograms are an imprecise guide to the site of earliest atrial excitation during retrograde slow pathway conduction.

Adolescent↗
PubMed2000

Association of follow-up change of left atrial appendage blood flow velocity with spontaneous echo contrast in nonrheumatic atrial fibrillation.

STUDY OBJECTIVES: To evaluate the time-related change of left atrial (LA) appendage flow velocity in chronic atrial fibrillation (AF) by follow-up transesophageal echocardiography (TEE) and to investigate its association with the occurrence of LA spontaneous echo contrast. DESIGN: Prospective follow-up study. SETTING: University-based, tertiary referral medical center. PATIENTS: Forty-seven patients with chronic nonrheumatic AF. INTERVENTIONS: All studied patients underwent both a baseline and follow-up TEE during a mean period of 13 +/- 7 months. MEASUREMENTS AND RESULTS: Baseline TEE revealed that LA spontaneous echo contrast was present in 28 patients (group 1) and was absent in 19 patients (group 2). The LA appendage flow velocity profiles at baseline were significantly lower in group 1 than in group 2; on follow-up, the appendage flow velocities decreased significantly in group 2, but were not significantly changed in group 1. Follow-up TEE revealed that spontaneous echo contrast was persistent in all group 1 patients. In group 2, LA spontaneous echo contrast was newly observed in 9 patients (group 2A) but was persistently absent in 10 patients (group 2B). In group 2A, all of the LA appendage flow velocity profiles decreased significantly at the follow-up study. In group 2B, however, only LA appendage inflow velocity integral showed significant decrease on follow-up; there were no significant changes in LA appendage outflow velocity indexes and peak inflow velocity. CONCLUSIONS: LA appendage flow velocity may decrease with time in some patients with AF, and this change is associated with a new occurrence of LA spontaneous echo contrast. For patients without LA spontaneous echo contrast, serial follow-up of the LA appendage flow velocity profiles may be useful for predicting future development of spontaneous echo contrast. Once LA spontaneous echo contrast occurs in AF patients, it tends to persist with time and the LA appendage is usually under a persistently low flow state.

Adult↗
PubMedDate not supplied

Technetium-99m glucarate uptake in a swine model of limited flow plus increased demand.

BACKGROUND: Glucarate is a 6-carbon dicarboxylic acid shown to be taken up by necrotic myocytes, binding to nuclear histones in animal models of coronary occlusion, resulting in infarction. This study investigated glucarate uptake in a model of severe ischemia. METHODS AND RESULTS: Thirty-five experiments were performed, in which a catheter-mounted stenosis (reducing lumen dimensions by 80%) was placed in the left anterior descending coronary artery (LAD) of an anesthetized, instrumented domestic swine and technetium-99m glucarate (GLU) was injected during the last minute of 5 minutes of pacing. Hemodynamic and blood flow measurements were performed at control, during pacing, and during recovery. The animals were killed; their hearts were stained with fluorescein dye and triphenyl tetrazolium chloride (TTC). Electron micography (EM; n = 6) and cell centrifugation (n = 7) were also performed. On the basis of net lactate production and severe blood flow reduction in the risk region (RR), ischemia with pacing developed in 25 animals. Fifteen of 25 animals showed tracer uptake in the RR on in vivo and ex vivo imaging (scan positive), and 10 were scan negative in the RR. Endocardial blood flow in the RR during pacing was 0.28+/-0.16 mL/g/min for scan-positive and 0.30+/-0.17 mL/g/min for scan-negative experiments (P = not significant [NS]). Transmyocardial net lactate extraction during pacing was -63%+/-44% for scan-positive and -53%+/-60% for scan-negative experiments (P = NS). Control and recovery heart rates were higher in scan-positive experiments (108+/-14 vs. 92+/-17, and 125+/-24 vs. 104+/-18, P<.02). Lactate extraction was lower during control and recovery in scan-positive animals (2+/-29 vs. 30+/-19, P = .03). Scan-positive animals had a more proximal stenosis position. Minimal necrosis was documented by means of TTC negative staining in 8 of 15 scan-positive experiments (comprising 10%+/-4.3% of RR area). EM or cell fractionation was performed in 5 of the 7 remaining scan-positive and TTC-positive hearts, and in those 5 experiments, necrosis was documented by means of EM in 2 and by means of cell fractionation in 3. CONCLUSIONS: Uptake of Tc-99m glucarate was seen in the RR in a swine model of ischemia severe enough to produce myocyte injury and early cell death.

Animals↗
PubMed1998

[First annual report of practitioners of interventional cardiology in private practice in Germany. Results of procedures of left heart catheterization and coronary interventions in the year 1996].

The German Society for Cardiac Angiography and Interventions in Private Practice has started a registry of cardiac procedures since 1996 in order to establish a standard for performance. Although quality management for the cath lab makes sense and is also legally required, there is no generally recommended infrastructure for quality assurance existing in Germany at this time. Therefore, the German Society of Cardiologists in Private Practice (BNK) initiated a project in 1994 to develop a computer program for paperless documentation of diagnostic cardiac catheterizations and coronary interventions (PTCA) using a minimal data set. In 1996, 8 private associated groups participated in this project. The (anonymous) analysis of 10,316 diagnostic cardiac catheterizations and 2597 PTCA yielded the following results: In 95% of the patients, diagnostic cardiac catheterization was performed using the femoral and in 5% the brachial/radial approach. The mean volume of administered contrast medium was 164 +/- 138 ml/patient. The mean LV-EF was greater than 50% in 58.4% of the patients and between 30% and 50% in 10.1%. Coronary artery disease was diagnosed in 69.6% of the patients and valvular/congenital heart disease in 8.5%. In 18.4% of the patients undergoing diagnostic cardiac catheterizations no significant heart disease was identified. Mortality in the cath lab as well as the rate of cerebral insults was 0.05%. In 22.9% and 19% of the patients PTCA and cardiac surgery respectively was recommended. In patients undergoing PTCA, stable angina was present in 74.4% and unstable angina in 13.1%. Of the total number of PTCA procedures, 5.8% were performed in the setting of acute myocardial infarction. The PTCA lesion success rate was 96%, the mean diameter stenosis was 81% pre and 6% post-intervention. The mortality rate at 1 month post-PTCA was 0.4%, and myocardial infarction 1.0%. An acute occlusion occurred in 1.3% of the PTCA patients; 0.6% had to be transferred for emergency bypass surgery. None of the cath labs had on-site surgery. In comparison to other registries, our data show some similarities but also some different trends. Thus, our newly developed software proved to be reliable, fast and easy to use. Participating centers receive immediate feedback regarding their position within the whole group.

Angiocardiography↗
PubMed1994

Delineation of determinants of left ventricular early filling. Saline versus blood infusion.

BACKGROUND: Left atrial pressure (LAP) is often believed to play a dominant role in the determination of left ventricular (LV) early diastolic filling. In a previous study we found no significant relation between LAP and LV early filling velocity (E) but found instead a relation between E and two determinants of LV myocardial shortening (contractility and afterload). To determine if such disparate results may be related to the data ranges of the independent variables in a given population of animals, we took advantage of the differential hemodynamic effects of two modes of volume expansion: saline and whole blood. METHODS AND RESULTS: Eighteen closed-chest anesthetized dogs were instrumented with micromanometers for measurement of LV, left atrial, and aortic pressures. LV volumes were obtained with use of contrast ventriculography, pressures by micromanometry, and transmitral flow-velocity by Doppler echocardiography. After obtaining baseline measurements, group 1 (n = 9) received rapid infusion of 500 to 650 mL of saline over 10 minutes, and group 2 (n = 9) received the same volume infusion of whole blood. In terms of two known determinants of E, infusion of saline resulted in a significant increase in LAP at the moment of mitral valve opening (X1) (1.5 +/- 0.9 to 5.7 +/- 1.4 mm Hg; P < .05) and a moderate decrease in the pressure decay rate during isovolumic relaxation (tau 1/2) (22.9 +/- 2.4 to 26.3 +/- 3.5 milliseconds; P < .05). When these two factors were entered together into a multiple regression analysis with E as the dependent variable, the overall correlation was found to be significant (R = .722; P < .008), with both independent variables contributing significantly to the relation. When factors related to myocardial shortening (afterload and contractility) were added to this relation, they did not significantly improve the prediction of E. Like saline, whole blood infusion augmented X1 (1.6 +/- 2.4 to 8.8 +/- 3.2 mm Hg; P < .05) and tau 1/2 (21.5 +/- 2.6 to 32.0 +/- 6.3 milliseconds; P < .05) but also significantly increased LV afterload as measured by aortic diastolic pressure (91 +/- 10 to 110 +/- 12 mm Hg; P < .05). Multiple regression analysis of X1 and tau 1/2 with E again revealed a significant relation (R = .761; P < .002), with both independent variables contributing significantly to the relation. However, in this case, addition of contractility and afterload to the regression significantly improved the relation (R = .909; P < .001), with all four independent variables now contributing significantly to the prediction of E. CONCLUSIONS: Combined with our previous results, this study indicates the degree to which experimental methods can have an impact on the delineation of the determinants of a phenomenon as complex as LV early diastolic filling. Which independent variables emerge as primary determinants can be strongly influenced by the experimenter's choice of experimental design and manipulations. Specifically, experiments using volume infusion to delineate the responses of the cardiovascular system to variations in loading must allow for the hemodynamic changes that are inherent in the choice of infusate and infusion technique, especially when those interventions may significantly alter blood oxygen-carrying capacity and, in turn, differentially modify factors that affect the magnitude of the early diastolic transmitral pressure gradient.

Animals↗
PubMed1997

The influence of oxidative stress on various inotropic responses in isolated rat left atria.

The effects of free radicals, generated by electrolysis of a physiological salt solution, on various inotropic responses to drugs in isolated rat left atria were studied. Evidence for the generation of hydroxyl radicals was obtained from an appropriate fluorimetric assay. The amount of free radicals produced by electrolysis of the medium proved current-dependent. Exposure of isolated rat left atria to the medium which had been subjected to electrolysis caused a current-dependent decrease in contractile force. Oxidative stress, as a result of the electrolysis of the medium, caused altered inotropic responses to extra cellular Ca2+ (pD2 control group: 2.62 +/- 0.06 vs. 2.44 +/- 0.07 electrolysis group), sodium withdrawal (rise in contractile force control group: 1.73 +/- 0.19 mN vs. 0.48 +/- 0.21 mN electrolysis group) and lowering of stimulation frequency. The response to isoprenaline was diminished in atria subjected to oxidative stress and led to a rightward shift of the concentration response curves (pD2 control group: 7.56 +/- 0.10 vs. 6.77 +/- 0.11 electrolysis group). In addition, the inotropic responses to forskolin (pD2 control group: 6.17 +/- 0.12 vs. < 4.5 electrolysis group) and dibutyryl cAMP (rise in contractile force caused by 1 x 10(-5) M db-cAMP in control group: 2.15 +/- 0.01 mN vs. 1.21 +/- 0.10 mN electrolysis group) proved blunted as well. Measurement of the adenylyl cyclase activity revealed that free radicals attenuated the basal (by 11.1%) and forskolin stimulated (155.0 +/- 5.1 vs. 48.0 +/- 1.8 pmol cAMP/mg prot./min for control and electrolysis group respectively) activity of the adenylyl cyclase. DMSO, a well known hydroxyl radical scavenger, was able to abolish the free radical-induced decrease in the response to isoprenaline. Surprisingly, addition of alpha-adrenoceptor agonists to atria subjected to electrolysis-generated free radicals led to a rapid decrease in contractile force. DMSO was unable to counteract the negative intropic effect of methoxamine in atria subjected to oxidative stress. This negative inotropic response to alpha-adrenoceptor agonists in atria subjected to electrolysed medium is unlikely to be the direct result of phospholipase C or protein kinase C activation. Angiotensin II (which stimulates PLC, as well) did not reduce contractile force and chelerythrine (a PKC inhibitor) was unable to counteract the negative inotropic effect of the adrenoceptor agonists. In addition, the negative inotropic effect of methoxamine proved insensitive to 10(-6) M phentolamine and 10(-5) M doxazosin, which indicates an alpha-adrenoceptor independent mechanism. From this study we conclude that free radicals alter responses to various inotropic stimuli. These alterations may be the result of injured contractile elements, transporter molecules and molecules involved in signal transduction. Addition of alpha-adrenoceptor agonists after oxidative stress leads to a alpha-adrenoceptor. PLC and PKC independent decrease in contractile force.

Adenylyl Cyclases↗
PubMed1997

Our tortuous heart in dynamic mode--an echocardiographic study of mitral flow and movement in exercising subjects.

Blood traces tortuous paths of flow through the heart. We postulate that momentum changes associated with direction changes optimize dynamic coupling between ventricular and atrial function, particularly on exercise. Traces of pulsed Doppler mitral flow and M-mode long-axis mitral ring movement were recorded before and during exercise, increased in 25-W steps to strenuous levels (146 +/- 30 W), in 16 healthy volunteers, aged 38 +/- 10 years. R-R intervals fell from 821 +/- 151 to 437 +/- 51 ms, and diastole from 458 +/- 134 to 169 +/- 33 ms. Peak mitral flow velocities rose from 0.68 +/- 0.17 to 1.27 +/- 0.16 m/s, and mitral valve ring displacements from 13.8 +/- 3.3 to 19.3 +/- 3.4 mm. Biphasic diastolic curves of flow and movement became monophasic as R-R fell below 500 ms, with atrial systole apparently coming to coincide with elastic ventricular recoil to give a single elevated peak of mitral flow. The increased slope and amplitude of Doppler curves indicate increased rates of change of momentum, which imply enhanced inertial forces. The illustrated patterns of flow and movement on exercise accord with the postulated "dynamic" mode of function, in which forces between atria, ventricles, and passing blood masses become tightly coupled to achieve a sling-like redirection of momentum through tortuous paths of flow, but more extensive data are needed to adequately model and quantify inertial force exchanges of the exercising heart.

Adult↗
PubMed1990

Placement of esophageal stethoscope by acoustic criteria does not consistently yield an optimal location for the monitoring of core temperature.

The esophageal stethoscope has evolved into a device for both acoustic and core temperature monitoring. To test whether routine placement according to acoustic criteria results in placement of the core temperature sensor in the region of contiguity between the esophagus and the heart, we determined the depth of placement electrocardiographically. All patients were undergoing nonthoracic elective operations requiring general anesthesia and tracheal intubation. First, we established that different observers selected the same esophageal depth within +/- 1 cm electrocardiographically, using the criterion of a symmetric biphasic P wave of maximal amplitude (7 patients). Then, in 30 more patients, we compared routine acoustic placements with the depths of the maximal-amplitude biphasic P wave. Stethoscopes placed according to acoustic criteria were within +/- 3 cm of P-wave depths in 15 of 30 patients. In the remaining patients, measured discrepancies ranged up to 13.5 cm. We conclude that the prevailing stethoscope design, with a thermistor at the tip, below the acoustic window, does not ensure placement of the thermistor within the optimal region for monitoring of core temperature. A modification in design that would take advantage of the reliability of electrocardiographic positioning is suggested.

Acoustics↗
PubMed1990

Balloon valvuloplasty for mitral restenosis after previous surgery: a comparative study.

We studied 203 patients with mitral stenosis treated by transarterial valvuloplasty. Forty two (group A) had undergone closed (n = 30) or open n = 12) surgical commissurotomy 15 +/- 5 years before. The remaining 161 had not undergone previous surgery (group B). There were no significant differences between both groups in terms of age, sex, functional class, left atrial size, two-dimensional anatomic features of the valve, incidence of mild basal mitral regurgitation, or ejection fraction. A comparative analysis of both groups showed no significant differences in terms of changes in the mean gradient, mitral valve area, and incidence of severe postvalvuloplasty mitral regurgitation (9.5% versus 5.5%). Echo-Doppler follow-up studies (11 +/- 7 months) showed persistent gradient relief in either group. We conclude that the immediate and short-term results of balloon valvuloplasty in patients who had undergone previous surgery are similar to those observed in patients who had not had commissurotomy.

Catheterization↗
PubMed1988

Correlation of minimum coronary lumen diameter with left ventricular functional impairment induced by atrial pacing.

To understand whether quantitative measurement of minimal coronary luminal diameter is a better method than percent diameter narrowing for assessing the functional impairment of myocardial contractility produced by coronary artery stenoses, measurements were made from 37 stenotic segments in 27 patients with coronary artery disease and from corresponding segments in 10 subjects without coronary artery narrowing. An assessment of the reliability of the 2 types of measurements was made by correlating them with the physiologic parameters of both segmental wall motion and global ejection fraction response induced by atrial pacing. Digitally acquired coronary angiograms were used to facilitate quantitative analysis. Measurements by edge detection and videodensitometry correlated closely (r = 0.94). Percent diameter narrowing correlated moderately with the change in ejection fraction (r = -0.41) or with the change in segmental wall motion (r = -0.44). The measurement of minimal lumen diameter correlated with the change in global ejection fraction (r = 0.61) and did so even better with the change in segmental wall motion (r = 0.78, p less than 0.05). A minimal lumen diameter of less than or equal to 1.5 mm identified patients likely to have a functional impairment during atrial pacing as assessed by either global ejection fraction or segmental wall motion defects. We conclude that minimal coronary luminal diameter provides a better method than percent diameter narrowing calculations to measure the anatomic severity of coronary artery narrowing.

Angiography↗