Showing papers on "Ventricle published in 1993"
TL;DR: It is indicated that stretch stimulates both ANP and BNP secretion from hypertropic ventricular myocytes, and the results suggest that protein kinase-C may be involved in stretch-induced ventricular ANP release, whereas the influx of extracellular calcium may not be necessary.
Abstract: Ventricular hypertrophy is characterized by augmentation of the synthesis and storage of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). To evaluate in vitro the cellular mechanisms of immunoreactive ANP (IR-ANP) and BNP (IR-BNP) release from ventricular cardiocytes, we measured the secretory response to graded passive myocardial stretch in isolated atrialectomized perfused hypertrophied hearts of 14- to 18-month-old spontaneously hypertensive rats. At this age, the ventricular levels of both IR-ANP and IR-BNP were markedly higher in spontaneously hypertensive (182 +/- 27 and 32 +/- 3 pmol/ventricle, respectively) than in age-matched normotensive Wistar-Kyoto rats (35 +/- 4 and 12 +/- 1 pmol/ventricle, respectively; P < 0.001), whereas the differences between the strains in atrial levels of these peptides were small. The release of natriuretic peptides from ventricles in response to stretch was examined by increasing the volume of the intraventricular balloon for 10 min. Stretching of the hypertrophied ventricles produced a rapid transient (from 1-5 min) increase in both IR-ANP and IR-BNP secretion. As left ventricular pressure rose from 0 to 26 +/- 1 mm Hg, IR-ANP and IR-BNP release into the perfusion fluid increased 1.8 +/- 0.4- and 2.5 +/- 0.2-fold, respectively. Infusion of staurosporine, known to inhibit protein kinase-C activity in heart cells, blocked the stretch-induced increase in IR-ANP release (F = 3.10; P < 0.001, by analysis of variance), but had no effect on basal ventricular IR-ANP secretion (F = 0.87; P = NS). An L-type calcium channel antagonist, diltiazem, had no significant effect on basal (F = 1.20; P = NS) or stretch-stimulated (F = 1.47; P = NS) IR-ANP release from hypertrophied rat myocardium. Chromatographical analysis revealed that the ventricles primarily release the active processed 28- and 45- amino acid ANP- and BNP-like peptides, respectively, both before and during stretch. This study indicates that stretch stimulates both ANP and BNP secretion from hypertropic ventricular myocytes. The results further suggest that protein kinase-C may be involved in stretch-induced ventricular ANP release, whereas the influx of extracellular calcium may not be necessary.
350 citations
TL;DR: It is suggested that endogenous ET-1 contributes to the progression of cardiopulmonary alterations in rats with MCT-induced pulmonary hypertension.
Abstract: Endothelin-1 (ET-1) is known to have potent contractile and proliferative effects on vascular smooth muscle cells and is known to induce myocardial cell hypertrophy. We studied the pathophysiological role of endogenous ET-1 in rats with monocrotaline-induced pulmonary hypertension. Four-week-old rats were given a single subcutaneous injection of 60 mg/kg monocrotaline (MCT rats) or saline (control rats) and were killed after 6, 10, 14, 18, and 25 days. In the MCT rats, right ventricular systolic pressure progressively increased and right ventricular hypertrophy developed in a parallel fashion. The venous plasma ET-1 concentration also progressively increased, and this increase preceded the development of pulmonary hypertension. The isolated pulmonary artery exhibited a significantly weaker response to ET-1 in the MCT rats on day 25 but not on days 6 and 14. In the MCT rats, the expression of prepro ET-1 mRNA as measured by Northern blot analysis significantly increased in the heart on days 18 and 25, whereas it gradually decreased in the lungs. The peptide level of ET-1 in the lungs also significantly decreased in the pulmonary hypertensive stage. The expression of prepro ET-1 mRNA had increased by day 6 only in the kidneys. Continuous infusion of BQ-123, a selective ETA receptor antagonist, by an osmotic minipump (14.3 mg per day per rat for 18 days) significantly inhibited the progression of both pulmonary hypertension (right ventricular systolic pressure, 77.8 +/- 4.2 [mean +/- SEM] mm Hg [n = 10] versus 52.3 +/- 2.4 mm Hg [n = 7]; P < .01) and right ventricular hypertrophy (right ventricle/[left ventricle +/- septum], 0.56 +/- 0.03 [n = 10] versus 0.41 +/- 0.02 [n = 7]; P < .01). Histological examination revealed that BQ-123 also effectively prevented pulmonary arterial medial thickening. The inhibition of right ventricular hypertrophy by BQ-123 may be partly ascribed to the blockade of excessive stimulation of the heart by ET-1, in addition to the prevention of pulmonary hypertension. The present findings suggest that endogenous ET-1 contributes to the progression of cardiopulmonary alterations in rats with MCT-induced pulmonary hypertension.
343 citations
TL;DR: Regional differences in action potential duration have important implications for the gradient of repolarisation in rat left ventricle, for the genesis of the T wave of the electrocardiogram, and for both electrical and mechanical restitution (refractoriness).
Abstract: Objective: The ionic mechanisms for differences in action potential waveforms in rat left ventricle were studied by recording L-type Ca2+ current, transient outward K+ current, and inwardly rectifying background K+ current in single myocytes. Methods: Single cells were obtained from adult rat hearts by enzymatic dispersion of tissue segments from the epicardium at the apex and the endocardium at the base of the left ventricle. Whole cell voltage clamp methods together with cell shortening measurements were used to identify the K+ currents involved in early and late repolarisation and to correlate changes in action potential shape with inotropic responses. 4-Aminopyridine was used to block the transient outward K+ current, It, to evaluate the contribution of this current to repolarisation. Results: Action potential recordings demonstrated that cells from endocardial tissue at the base of the left ventricle have a considerably longer action potential than those from epicardial tissue at the apex. 4-Aminopyridine had a much more pronounced action potential lengthening and inotropic effects on cells from epicardium than on myocytes from endocardium suggesting that It is larger in the epicardium. Voltage clamp measurements confirmed this. In contrast, the L-type Ca2+ current, the resting membrane potential, and the inwardly rectifying background K+ current were very similar in these two regions of left ventricle. Conclusions: One significant factor contributing to the heterogeneity of action potential waveforms in rat left ventricle is a differential distribution of a Ca+ independent transient outward K+ current, It. Regional differences in action potential duration have important implications for the gradient of repolarisation in rat left ventricle, for the genesis of the T wave of the electrocardiogram, and for both electrical and mechanical restitution (refractoriness).
Cardiovascular Research 1993; 27 :1795-1799
232 citations
TL;DR: The results demonstrate that acute hemodynamic embarrassment early after LV infarction is associated with augmented angiotensinogen gene expression.
193 citations
TL;DR: Myocardial infarction leads to impairment in the contractile behavior of the remaining cells and to the activation of Ang II receptors and effector pathway associated with these receptors, which may be involved in the reactive growth adaptation of the viable myocytes.
Abstract: To determine the effects of acute myocardial infarction on the regulation of angiotensin II (Ang II) receptors and contractile performance of left and right ventricular myocytes, coronary artery ligation was surgically induced in rats, and Ang II receptor density and affinity and the mechanical properties of surviving muscle cells were examined 1 week later. Physiological determinations of cardiac pump function revealed the presence of ventricular failure, which was associated at the cellular level with a depression in the velocity of myocyte shortening and relengthening, a prolongation of time to peak shortening, and a reduction in the extent of cell shortening. These abnormalities in single-cell function were more prominent in left than in right ventricular myocytes. Cellular hypertrophy was documented by increases in cell length and width, which were also greater in the spared myocytes of the infarcted left ventricle. Reactive hypertrophy was accompanied by a 1.84- and 1.85-fold increase in the density of Ang II receptors on left and right myocytes, respectively. On the other hand, the affinity of Ang II receptors for the radiolabeled antagonist was not altered. However, Ang II-stimulated phosphoinositol turnover was enhanced by 3.7- and 2.5-fold in left and right myocytes, respectively, after infarction. Ventricular myocytes were found to possess the AT1 receptor subtype exclusively. In conclusion, myocardial infarction leads to impairment in the contractile behavior of the remaining cells and to the activation of Ang II receptors and effector pathway associated with these receptors, which may be involved in the reactive growth adaptation of the viable myocytes.
187 citations
TL;DR: Electrocardiogram-gated spin echo NMR imaging of the heart may be used for quantitating right ventricular mass in normal subjects and in patients with primary pulmonary hypertension, in whom it may also provide an alternative noninvasive technique for estimating mean pulmonary artery pressure.
185 citations
Journal Article•
TL;DR: Left ventricular hypertrophy is the most common cardiovascular alteration observed in end-stage renal disease patients and progresses over the time on hemodialysis together with a progressive worsening of both systolic and diastolic functions.
175 citations
TL;DR: Doppler diastolic indexes in beta-thalassemia major patients with normal left ventricular systolic function are similar to those seen in conditions with an increased preload, probably because of chronic anemia.
Abstract: BACKGROUNDDiastolic left ventricular function expressed by diastolic Doppler characteristics of the left ventricle has never been properly investigated.METHODS AND RESULTSLeft ventricular inflow and pulmonary vein flow patterns were assessed by Doppler echocardiography in 88 beta-thalassemia major patients with normal left ventricular systolic function; 34 were young (age, 15.1 +/- 3.2 years) and 54 were adults (age, 25.1 +/- 3.6 years). The findings were compared with those obtained from 22 young (age, 13.8 +/- 2.4 years) and 24 adult (age, 25.3 +/- 4.1 years) normal individuals. In both groups of patients, peak flow velocities in early (E) and late (A) diastole were higher than in the control subjects (young E: P < .01; adult E: P < .001; young A: P < .05; adult A: P < .05), whereas no difference was found in the E/A ratio, deceleration time, or isovolumic relaxation time. Pulmonary vein systolic (S) and diastolic (D) velocities were also higher in beta-thalassemia major patients compared with the contr...
166 citations
TL;DR: Aside from its effect on systolic augmentation with a stimulated muscle wrap, cardiomyoplasty may have an important "girdling" effect on the left ventricle that prevents dilatation and deterioration of left ventricular function.
162 citations
TL;DR: The observations suggest that the cardiac renin-angiotensin system rather than the circulating system may play an important role in ventricular dilatation after myocardial infarction.
161 citations
Journal Article•
TL;DR: Diastolic function appears to be more sensitive for detection of abnormal left ventricular function in patients with aortic stenosis or to precede systolic dysfunction or both, and a reduction of circulating blood volume to reduce diastolic filling pressures, and thus dyspnea, is often indicated.
Abstract: Diastolic dysfunction is characterized by an increased resistance to filling with increased diastolic filling pressures. A variety of disorders are associated with diastolic dysfunction, such as hypertrophy, structural alterations of the myocardium with increased fibrosis, myocardial scarring, or infiltrative processes. In addition to these changes, physiological abnormalities of the left ventricle with impaired relaxation, decreased diastolic filling, and increased stiffness of the myocardium can be observed. In patients with aortic stenosis, the most common cause for diastolic dysfunction is left ventricular hypertrophy. Diastolic dysfunction is found in approximately 50% of the patients with normal systolic ejection performance and in 100% of the patients with depressed function. Diastolic function appears either to be more sensitive for detection of abnormal left ventricular function in patients with aortic stenosis or to precede systolic dysfunction or both. Treatment of diastolic dysfunction is usually achieved by aortic valve replacement with regression of left ventricular hypertrophy, but in patients with decompensated aortic stenosis, a reduction of circulating blood volume to reduce diastolic filling pressures, and thus dyspnea, is often indicated. Prognosis of patients with diastolic dysfunction is usually better than that of patients with systolic dysfunction but is clearly worse than that of normal patients.
TL;DR: MR imaging can be used to assess morphologic alteration, tissue abnormalities, and global as well as regional dysfunction of the right ventricle in patients with ARVD and may become a useful clinical tool for diagnosing and grading ARVD.
Abstract: Arrhythmogenic right ventricular disease (ARVD) is increasingly found in young adults with ventricular arrhythmias and is characterized by ventricular tachycardia originating within the right ventricle and regional or diffuse abnormalities in the contraction of the right ventricle. Until now, the gold standard for the detection of global and regional abnormalities of the right ventricular wall has been angiography combined with biopsy. The purpose of the current study was to compare MR imaging with angiography for assessing the location and extent of morphologic and functional abnormalities in patients with ARVD.Electrocardiographically gated spin-echo and cine gradient-echo MR imaging of the heart was performed in 36 consecutive patients with biopsy-proved ARVD. Patients were prospectively separated into two groups according to the results of invasive electrophysiologic tests (18 with inducible ventricular tachycardia during invasive electrophysiologic studies [ARVD 1] and 18 without inducible ventricula...
TL;DR: The cardiac manifestation of Becker muscular dystrophy is characterized by early right ventricular involvement associated or not with left ventricular impairment, and exon 49 deletion is associated with cardiac disease.
TL;DR: The left ventricle seems to be activated much more rapidly with right ventricular pacing than with left bundle branch block, and Electromechanical delay, contraction and relaxation times, and extent of incoordinate ventricular wall motion differ strikingly between the two conditions.
Abstract: OBJECTIVE--To compare the different effects of right ventricular pacing and classic left bundle branch block on left ventricular function. DESIGN--Retrospective and prospective study of 48 patients by electrocardiography, and M mode, cross sectional, and Doppler echocardiography. SETTING--A tertiary cardiac referral centre. PATIENTS--48 patients (age range 21 to 89 years, 15 women), 24 with a VVI pacemaker implanted and 24 with classic left bundle branch block. Functional mitral regurgitation was present in all those with right ventricular pacing and 22 of those with left bundle branch block. RESULTS--Age, RR interval, and left ventricular size were similar in the two groups, as were conventional measurements of overall systolic function: shortening fraction and pre-ejection and aortic ejection times. In right ventricular pacing, however, QRS duration (p < 0.01) and electromechanical delay were much longer (p < 0.001), whereas the time intervals from onset of mitral regurgitation to aortic opening (contraction time) and from A 2 to the end of mitral regurgitation (relaxation time) were consistently shorter (p < 0.01) than corresponding values in patients with left bundle branch block. Reversed splitting of the second heart sound was much commoner in left bundle branch block (p < 0.02), and only these patients showed an early systolic ventricular septal contraction. Its onset followed the initial deflection of the QRS complex by 40(15) ms and preceded mitral regurgitation by a small but consistent interval of 10 ms (p < 0.01). The onset of posterior wall thickening was synchronous with the onset of mitral regurgitation in right ventricular pacing but much later (p < 0.01) in patients with left bundle branch block. The extent of incoordinate wall motion measure as relative dimension change during pre-ejection and isovolumic relaxation period was much greater (p < 0.01) in left bundle branch block. These major differences were not altered by left ventricular cavity size in either group, nor by the presence of previous left bundle branch block in patients who were subsequently paced. CONCLUSIONS--The left ventricle seems to be activated much more rapidly with right ventricular pacing than with left bundle branch block. This applies even when left bundle branch block is present before pacing. Electromechanical delay, contraction and relaxation times, and extent of incoordinate ventricular wall motion differ strikingly between the two conditions. The use of right ventricular pacing as an experimental model of left bundle branch block in humans must be re-examined.
TL;DR: In this paper, the authors examined the ability of the left ventricle to accommodate an increase in preload (Frank-Starling mechanism) in the presence of congestive heart failure (CHF) but in the absence of the complicating effects of hypertrophy and fibrosis.
Abstract: The goal of this study was to elucidate the ability of the left ventricle to accommodate an increase in preload (Frank-Starling mechanism) in the presence of congestive heart failure (CHF) but in the absence of the complicating effects of hypertrophy and fibrosis. To accomplish this, the effects of volume loading were examined in eight conscious dogs during the control state and after 3 wk of right ventricular pacing (240 beats/min). CHF increased heart rate (by 16 +/- 5 from 92 +/- 5 beats/min), left ventricular (LV) end-diastolic pressure (by 17 +/- 2 from 10 +/- 1 mmHg), and LV end-diastolic volume (EDV; by 23 +/- 4 from 57 +/- 3 ml). Despite reduced LV ejection fraction (from 54 +/- 3 to 31 +/- 3%), there was no significant change in cardiac output (2.5 +/- 0.3 l/min) compared with control (2.7 +/- 0.2 l/min). Stroke volume was preserved (control 19 +/- 2 ml; CHF 18 +/- 2 ml) at a constant heart rate by a shift to the right in the relationship between LV stroke volume and EDV, indicating the importance of chronic ventricular dilatation in maintaining pump performance. In the control state, acute volume load increased LV EDV (by 17 +/- 2 ml) and stroke volume (by 11 +/- 2 ml), whereas in CHF it did not increase LV EDV or stroke volume. Scanning electron microscopy revealed areas of reduced collagen weave pattern surrounding myofibers. Myocyte cross-sectional area by transmission electron microscopy was significantly reduced, and there were multiple electron-dense expansions of the Z lines with disruption of the normal lateral sarcomere alignment. These morphological findings suggest that chronic ventricular dilatation utilized in CHF results from myocyte stretch and morphological intracellular rearrangement. Furthermore, the failing heart cannot further augment stroke volume by acutely increasing EDV in CHF, suggesting that the Frank-Starling reserve is essentially exhausted.
TL;DR: Findings indicate that the production of ET‐1 increased in the hypertrophied left ventricle of aorta‐banded rats, thereby suggesting the possible involvement of endogenous ET‐ 1 in the development of cardiac hypertrophy due to pressure overload.
TL;DR: Improved understanding of myocardial relaxation at the cellular level and delineation of the molecular regulation of myocyte hypertrophy and fibroblast proliferation may lead to new and innovative approaches to the treatment of heart failure.
TL;DR: Magnetic resonance (MR) velocity mapping offers the major advance of simultaneous quantification of regurgitant volume in cases of concomitant regurgitation and has potential to become a clinical tool in assessment of severity in aortic stenosis.
TL;DR: MRI clearly identifies wall motion dynamics and provides calculations of segmental wall thickening and haemodynamic parameters and Dobutamine is a useful stress agent by virtue of its safety, operator control and its effects which resemble physical exercise.
Abstract: Magnetic resonance imaging (MRI) provides high-resolution images of the heart. However, physical exercise during MRI is difficult due to space restriction and motion artefacts. To evaluate the feasibility of MRI during stress conditions, dobutamine was used as an alternative to exercise. Haemodynamics, ventricular volumes and wall thickening were measured at rest and during peak dobutamine infusion (15 micrograms.kg-1 x min-1) in 23 normal human subjects. To calculate left ventricular volumes, eight short-axis views were obtained encompassing the left ventricle from base to apex. At six levels, percent systolic wall thickening (%WTh) was measured in 18 segments (20 degrees intervals). Heart rate, systolic and diastolic blood pressures, stroke index, cardiac output and left ventricular ejection fraction increased significantly during dobutamine infusion (all P values < 0.001). In addition, %WTh increased significantly (P < 0.001) during dobutamine compared to the control state at all levels except in the apical and low-left ventricular levels. Both in control conditions and during dobutamine, segmental wall motion analysis showed the highest %WTh at the posterolateral area and the lowest %WTh at the septal region (P < 0.05). MRI clearly identifies wall motion dynamics and provides calculations of segmental wall thickening and haemodynamic parameters. Dobutamine is a useful stress agent by virtue of its safety, operator control and its effects which resemble physical exercise.
TL;DR: The present data suggest that peripheral plasma BNP and ANP levels are useful noninvasive indices of cardiac performance.
Abstract: The present study was designed to investigate whether brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations correlate with left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), diastolic pulmonary arterial pressure (DPAP), right atrial pressure (RAP), or ejection fraction (EF). Plasma BNP and ANP levels were determined by commercial radioimmunoassays (Peninsula) after Sep Pak C18 extraction in blood samples withdrawn from the pulmonary artery and the left ventricle or from the left ventricle and the femoral vein in 85 patients undergoing diagnostic cardiac catheterization. Linear and nonlinear regression analysis and the paired sample t-test were applied to the data. Pulmonary arterial plasma BNP and ANP levels showed a close nonlinear correlation with LVEDP (BNP: r = 0.94, p < 0.001; ANP: r = 0.81, p < 0.001), a significant linear correlation with PCWP, DPAP, and RAP, and a significant negative correlation with EF. ANP concentrations decreased significantly from the pulmonary artery to the left ventricle and from the left ventricle to the femoral vein (p < 0.001). BNP levels also decreased significantly between the left ventricle and the femoral vein (p < 0.001), but there was no significant difference between pulmonary arterial and left ventricular BNP concentrations. BNP and ANP concentrations correlated significantly between pulmonary arterial and left ventricular blood samples (BNP: r = 0.99, ANP: r = 0.93, p < 0.001) and between left ventricular and peripheral blood samples (BNP: r = 0.99, ANP: r = 0.94, p < 0.001). The present data suggest that peripheral plasma BNP and ANP levels are useful non-invasive indices of cardiac performance.
TL;DR: Late failure of the systemic right ventricle is seen in up to 10% of patients after atrial switch for transposition of the great arteries and in patients with atrioventricular and ventriculoarterial discordance, and 16 patients have had an arterial switch with atrial reconstruction.
TL;DR: In most patients, cardiac tamponade should be diagnosed by a clinical examination that shows elevated systemic venous pressure, tachycardia, dyspnea, and paradoxical arterial pulse and by echocardiographic demonstration of moderately large or large circumferential pericardial effusion.
Abstract: In most patients, cardiac tamponade should be diagnosed by a clinical examination that shows elevated systemic venous pressure, tachycardia, dyspnea, and paradoxical arterial pulse. Systemic blood pressure may be normal, decreased, or even elevated. The diagnosis is confirmed by echocardiographic demonstration of moderately large or large circumferential pericardial effusion and in most instances, of right atrial compression, abnormal respiratory variation in right and left ventricular dimensions, and in tricuspid and mitral valve flow velocities. Pulsus paradoxus may be absent with left ventricular dysfunction, atrial septal defect, regional tamponade, and positive-pressure breathing. Systemic venous pressure may be normal with localized tamponade of the left atrium or ventricle. Patients with moderately large or large pericardial effusions may have echocardiographic evidence of right atrial compression without clinical signs of elevated venous pressure or pulsus paradoxus. The majority of these patients have mild or moderate tamponade and if not subjected to pericardial drainage, should be observed closely. In some of these patients, when the etiology is known and the disease can be treated effectively with medication, e.g., nonsteroidal anti-inflammatory agents or adrenal corticosteroids in Dressler's syndrome or relapsing pericarditis, pericardial drainage may not be necessary.
TL;DR: Overall, left ventricular end-diastolic and end-systolic chamber volumes increase progressively from hospital discharge to 1 year after an initial transmural myocardial infarction in patients with a moderately large anterior wall infarctions but remain stable in Patients with a small inferior wall Infarction.
TL;DR: Evidence is provided for a decline in myocardial energy store and energy producing ability associated with the development of cardiac failure in rats with heart failure following coronary artery ligation.
TL;DR: Two fetuses, one with pulmonary atresia and the second with severe cardiovascular dysfunction, demonstrated an abnormal ductus venosus index associated with absent flow velocity during atrial systole, associated with notching in the umbilical vein.
Abstract: This study was designed to examine ventricular preload by measuring the ductus venosus index during the second trimester of pregnancy. A total of 137 women were entered into the study. Each fetus was examined with real-time, color and pulsed Doppler ultrasound. The color Doppler maximal velocity setting was adjusted so that the umbilical vein was homogeneous in color, did not demonstrate aliasing, and filled the venous lumen. The pulsed Doppler gate was placed within the ductus venosus in all subjects. Color Doppler identified a turbulent flow velocity within the ductus venosus which was not present in the umbilical vein, hepatic vein or inferior vena cava. The ductus venosus pulsed Doppler waveform demonstrated flow velocity from the umbilical vein to the heart during ventricular systole, the rapid filling phase of ventricular diastole, and atrial systole. However, flow velocity was decreased during atrial systole compared to ventricular systole and the rapid filling phase of diastole. The ductus venosus index was computed from the Doppler waveform of the ductus venosus at points consistent with ventricular and atrial systole ((ventricular systole - atrial systole)/ventricular systole). Regression analysis demonstrated a significant (p = 0.001) relationship between the ductus venosus index and gestational age (ductus venosus index = 75.5757 - 7.25484 x weeks gestation), standard error of the estimate = 7.21959; R = -0.451. One fetus with a hypoplastic left atrium and ventricle demonstrated a normal ductus venosus index. Two fetuses, one with pulmonary atresia and the second with severe cardiovascular dysfunction, demonstrated an abnormal ductus venosus index associated with absent flow velocity during atrial systole. This was associated with notching in the umbilical vein. The ductus venosus index is an angle-independent measurement from which right ventricular preload may be evaluated.
TL;DR: These results demonstrate that application of the 62-lead instead of the 12-lead ECG during endocardial pace mapping enhances the localization resolution of this mapping technique and enables more precise identification of the site of arrhythmogenesis in the majority of compared postinfarctionVT episodes.
Abstract: BACKGROUNDThe purpose of this study was to assess the value of body surface mapping and the standard 12-lead ECG in localizing the site of origin of postinfarction ventricular tachycardia (VT) during endocardial pace mapping of the left ventricle.METHODS AND RESULTSSimultaneous recordings of 62-lead body surface QRS integral maps and scalar 12-lead ECG tracings were obtained in 16 patients with prior myocardial infarction during a total of 26 distinct VT configurations and during subsequent left ventricular catheter pace mapping at 9 to 24 different endocardial sites. Anatomic pacing site locations were computed by means of a biplane cineradiographic method and plotted on a polar projection of the left ventricle. The QRS integral map and the QRS complexes of the 12 standard leads of each VT morphology obtained in a particular patient were compared independently with the different paced QRS integral maps and paced QRS complexes of the 12-lead ECG generated in that same patient. The stimulus site locations ...
TL;DR: The descending limb of the Doppler-derived mitral regurgitation velocity signal can be used as a semiquantitative estimate of the rate of ventricular relaxation in humans by comparing it with simultaneous high-fidelity left ventricular pressure measurements in humans.
Abstract: BACKGROUNDThe instantaneous pressure gradient between the left ventricle and left atrium during systole can be calculated from the mitral regurgitation Doppler velocity curve. The purpose of our study was to determine the accuracy of measuring the time constant of relaxation (TAU) derived from the Doppler mitral regurgitation signal by comparing it with simultaneous high-fidelity left ventricular pressure measurements in humans.METHODS AND RESULTSTwenty-five patients had continuous-wave Doppler mitral regurgitation recordings performed with simultaneous high-fidelity left ventricular pressure measurements. Fifteen of these patients had measurements of six to eight beats at various RR intervals. Doppler velocity curves were converted to left ventricular pressure curves by different methods through application of the modified Bernoulli equation at 3-msec intervals. The correlation between catheter-derived and Doppler-derived TAU was best when a zero asymptote and knowledge of the left ventricular end-diasto...
TL;DR: Patients with false aneurysms of the left ventricle do well after surgical repair, except when concomitant mitral valve replacement is necessary, except for patients who had severe mitral regurgitation before the operation.
TL;DR: The relationship between cross-sectional area and left ventricular volume was predominantly linear and varied little during isovolumic contractions in the normal canine left ventricle.
Abstract: The objective of this study was to determine the relationship of on-line measurements of left ventricular cavity area generated by echocardiographic automated border detection to true volume measured by an intraventricular balloon in an isovolumically contracting isolated canine heart preparation. Seven excised dog hearts had placement of an intraventricular balloon and were perfused in an ex vivo apparatus. Left ventricular area data from the midventricular short-axis plane and pressure data were recorded on a computer through a customized hardware and software interface with the ultrasound system. Left ventricular volumes were varied from 5 ml to maximal values (30 to 40 ml) at 1- ' ' 'ter increments. Three increasing and decreasing volume ramps were analyzed on each of seven hearts for a total of 1260 simultaneous measurements. Linear regression analysis correlated mean automated border detection area with absolute volume from each preparation. A predominantly linear relationship was observed with an average correlation of r = 0.97 ( y = 0.16 x - 0.69, SEE=0.31 cm 2 , p 2 ) but did show a systematic cardiac cycle-related variability in one dog (28% change in area, maximum to muumum, over all volumes). In conclusion, the relationship between cross-sectional area and left ventricular volume was predominantly linear and varied little during isovolumic contractions in the normal canine left ventricle. Echocardiographic automated border detection appears to be a promising method to reflect changes in left ventricular volume.
TL;DR: Depersion in refractoriness across the ischaemic border increased by 14-59% in individual hearts following sympathetic stimulation during acute, regional ischaemia, which may enhance the chance for regional conduction block and the propensity to re-entrant arrhythmias.
Abstract: Objective: Dispersion in refractoriness is considered a major factor in induction and persistence of cardiac arrhythmias. The sympathetic nervous system is known to modulate refractoriness. An index of refractoriness has therefore been assessed in normal and ischaemic myocardium simultaneously at multiple sites, with and without sympathetic stimulation. Methods: In six dogs on total cardiopulmonary bypass the average interval between local activations was measured during artificially induced ventricular fibrillation from extracellular electrograms simultaneously recorded from 32 ventricular sites. These local ventricular fibrillation intervals may be used as an index of local refractoriness. Results: During regional ischaemia, ventricular fibrillation intervals of ischaemic sites could prolong by up to 60% after 3 min following coronary occlusion. Left stellate ganglion stimulation during ischaemia produced either no response or prolonged the ventricular fibrillation intervals even further at ischaemic sites, whereas ventricular fibrillation intervals at non-ischaemic sites shortened. Dispersion in refractoriness across the ischaemic border increased by 14-59% in individual hearts following sympathetic stimulation during acute, regional ischaemia. Conclusions: Due to opposite effects on normal and ischaemic myocardium, sympathetic stimulation increases the difference in refractoriness over the ischaemic border. This may enhance the chance for regional conduction block and the propensity to re-entrant arrhythmias.
Cardiovascular Research 1993; 27 :1954-1960