Nonsurgical infarctectomy in acute experimental myocardial infarction

This study examines whether a catheter mounted left intraventricular balloon may prevent left ventricular (LV) dysfunction following acute experimental myocardial infarction. In 10 anesthetized pigs, multiple coronary arterial ligations were applied around the apex of the heart. LV end-diastolic pressure (LVEDP), aortic flow (AF), and LV long and short axis fractional shortening (FS) were measured before and at 15 min intervals after ligations. At the 60th min after ligation, the LV long axis FS and AF decreased by 7.2 +/- 2.6% (p < 0.05) and 13.25 +/- 2.68% (p < 0.01), respectively, and the LVEDP increased by 4.3 +/- 1.1 mm Hg (p < 0.01) while no change was noted in the LV short axis FS. An intraventricular catheter mounted nonpulsating balloon was positioned over the endocardium of the infarcted area at the LV apex. Inflation of the nonpulsating balloon to an optimal volume, which was found to be equal to 8-10% of the LV end-diastolic volume, resulted in a reduction (by 3.8 +/- 1.2 mm Hg, p < 0.01) of the already increased LVEDP and in an increase (by 6.6 +/- 2.1%, p < 0.05) in the LV short axis FS while no statistically significant change was noted in the AF and LV long axis FS. It is concluded that an intraventricular catheter mounted balloon patch positioned over the endocardium of the infarcted area may ameliorate early LV dysfunction, possibly by interfering with the functional geometry of the LV contraction.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Effect of inferior vena cava occlusion on left ventricular end-systolic pressure-volume relations in intact canine hearts--modulation by the autonomic nervous system

The effect of inferior vena cava occlusion (IVCO) on end-systolic pressure-volume relations (ESPVR) of the left ventricle was studied in intact canine hearts. In 12 anesthetized open-chest dogs, left ventricular (LV) pressure and volume were measured simultaneously using a microtip catheter and a conductance catheter, respectively. ESPVR was constructed from LV pressure-volume loops during IVCO (10 sec) and subsequent IVCO release under 5 conditions: control, after righ or left cardiac sympathetic nerve (CSN) stimulation, bilateral vagotomy (VAT), and both VAT and bilateral CSN resection. Emax in IVCO release was significantly greater than that in IVCO in the control state. Following right or left CSN stimulation, Emax was increased increased in both IVCO and IVCO release, with the same hysteretic change in Emax. With VAT, however, no hysteretic change was observed because Emax was the same in IVCO and IVCO release. After VAT and CSN resection, Emax was decreased in both IVCO and IVCO release, and again no hysteretic change was observed. These data imply that a sudden decrease in venous return into the heart induces a decrease in afferent vagal nerve activity, and thus increases efferent CSN activity, resulting in enhanced myocardial contractility.     

Effect of chronotropic and inotropic stimulation on the coronary pressure-flow relation in left ventricular hypertrophy

Left ventricular hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during increased cardiac work. The present study was performed to study the effects of chronotropic and inotropic stimulation on the coronary pressure-flow relation of the hypertrophied left ventricle of dogs and to determine the individual contributions of increases in heart rate and contractility to the exaggerated exercise-induced increases in effective back pressure (pressure at zero flow; Pzf). Ascending aortic banding in seven dogs increased the LV to body weight ratio to 7.7 +/- 0.3 g/kg compared to 4.8 +/- 0.2 g/kg in 10 normal dogs (p < or = 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. During resting conditions maximum coronary blood flow in the pressure overloaded hypertrophied left ventricle was impaired by both an increase in Pzf (25.1 +/- 2.6 vs 13.8 +/- 1.2 mmHg in hypertrophied vs normal ventricles, respectively, p < or = 0.01) and a decrease in maximum coronary conductance (slope of the linear part of the pressure-flow relation, slopep > or = linear) (8.6 +/- 1.1 vs 12.7 +/- 0.9 ml/min/mmHg, p < or = 0.01). Right atrial pacing at 200 and 250 beats/min resulted in similar rightward shifts of the pressure-flow relation in hypertrophied and normal hearts with 3.1 +/- 0.8 and 4.7 +/- 0.8 mmHg increases in Pzf in LVH and normal dogs, respectively; stepwise multivariate regression analysis indicated that the exaggerated decrease in filling pressure (10 +/- 2 vs 6 +/-2 mmHg) and decrease in left ventricular systolic pressure (45 +/- 5 vs 3 +/- 3 mmHg, p < or = 0.01) may have blunted a greater rightward shift of the pressure-flow relation produced by atrial pacing in the hypertrophied hearts. Inotropic stimulation with dobutamine (10-20 micrograms/kg/min, i.v.) resulted in minimal flow changes in normal hearts but produced a 4.4 +/- 1.5 mmHg (p < or = 0.05) rightward shift of the pressure-flow relation in hypertrophied hearts. which correlated with a greater increase in left ventricular systolic pressure (83 +/- 16 vs 18 +/- 4 mmHg. p < or = 0.05). Exercise resulted in a rightward shift in both normal and hypertrophied left ventricles, but the increase in Pzf was significantly greater in the hypertrophied hearts (15.2 +/- 0.9 vs 10.3 +/- 0.9 mmHg. p < or = 0.05). Stepwise multivariate regression analysis indicated that not only increases in left ventricular filling pressure, but also increases in heart rate and LV systolic pressure contributed to the abnormally great increase in effective coronary back pressure which results in limitation of myocardial perfusion during exercise in the pressure overloaded hypertrophied left ventricle.     

The effect of left ventricular pressure or volume overload on ventricular dimension in children. Left ventricular volume determination from one or two ventricular dimensions

The effect of pressure or volume overload on the geometry of the left ventricle (LV) was determined in order to examine the feasibility and accuracy of LV volume determinations from one minor axis or two dimensions (one minor axis and the longest length). The longest length (LL) and minor axis (MA) in both the anteroposterior (AP) view and lateral (LAT) view were determined from the LV cine silhouette in patients with normal LV volume and pressure (group 1), LV pressure (LVP) overload group (LVP greater than 140 mm Hg, group 2), and LV volume overload group (LV end-diastolic volume greater than 124% of normal, group 3). The ratio of the MA to the LL, which represents the spherical configuration of the LV, was less than "normal" in group 2, and higher than "normal" in group 3. In all groups the LV was less spherical at end-systole than at end-diastole. Additionally, the (MA)3 had a different relationship to true LV volume (biplane LV volume) in the three groups and from diastole to systole in each group. Left ventricular volume calculation from one minor axis was associated with a large error. In contrast, left ventricular volume can be accurately determined from two ventricular dimensions using either the anteroposterior or lateral ventricular image (r larger than or equal to 0.97).     

Effects of cardiomyoplasty on right ventricular filling during volume loading

BACKGROUND: Although cardiomyoplasty (CMP) is thought to improve ventricular systolic function, its effects on ventricular diastolic function are not clear. Especially the effects on right ventricular diastolic filling have not been fully investigated. Because pericardial influences are more pronounced in the right ventricle than in the left ventricle, CMP with its external constraint may substantially impair right ventricular diastolic filling. METHODS: Fourteen purebred adult beagles were used in this study. Seven underwent left posterior CMP, and 7 underwent a sham operation with a pericardiotomy and served as controls. Four weeks later, the hemodynamic effects of CMP were evaluated by heart catheterization before and after volume loading (central venous infusion of 10 mg/kg of 4.5% albumin solution for 5 minutes). RESULTS: In the CMP group, mean right atrial pressure and right ventricular end-diastolic pressure increased significantly from 3.1 +/- 1.2 mm Hg to 6.1 +/- 2.0 mm Hg (p < 0.001) and from 4.0 +/- 1.8 mm Hg to 9.6 +/- 2.5 mm Hg (p < 0.001), respectively. Volume loading in the control group did not significantly increase either variable. Right ventricular end-diastolic volume and stroke volume did not change significantly (from 53 +/- 9.3 mL to 60 +/- 9.0 mL and from 20 +/- 2.3 mL to 21 +/- 3.2 mL, respectively) in the CMP group. In the control group, however, right ventricular end-diastolic volume and stroke volume increased significantly from 45 +/- 7.7 mL to 63 +/- 14 mL (p < 0.05) and from 18 +/- 4.3 mL to 22 +/- 4.2 mL (p < 0.05), respectively. CONCLUSIONS: These results suggest that CMP may reduce right ventricular compliance and restrict right ventricular diastolic filling in response to rapid volume loading because of its external constraint.     

Preoperative assessment of esophageal pathology

Sodium pentobarbital (PB), 30 mg/kg, iv, was administered to 30 conscious dogs instrumented for measurement of cardiac output and regional blood flow distribution, left ventricular (LV) diameter, LV pressure, dP/dt, and dD/dt, i.e., velocity of myocardial fiber shortening. Ventilation was controlled during anesthesia to maintain arterial blood gases at control values for conscious dogs. The anesthetic produced an initial transient, peripheral vasodilation but the steady state effects 15-30 minutes later were characterized by slight reductions in mesenteric flow and cardiac output and increases in mesenteric and systemic resistances, whereas iliac and renal resistances were not significantly different from control. When heart rate rose, PB increased end-systolic diameter and decreased coronary resistance, LV end-diastolic diameter, dP/dt/P (42%), and shortening velocity (36%). When heart rate was controlled, PB still increased end-systolic diameter and decreased shortening velocity and dP/dt/P, as occurred during spontaneous rhythm, but end-diastolic diameter rose instead of falling and coronary resistance did not change. After recovery from bilateral cervical section of both carotid sinus and aortic nerves, PB failed to elicit tachycardia. Thus, PB affects systemic and regional hemodynamics only slightly, but depresses the myocardium markedly. The tachycardia associated with PB anesthesia in intact, trained dogs appears not to be only vagolytic, as previously thought, but is predominantly mediated through the arterial baroreceptor reflex.     

A novel monoclonal antibody permitting recognition of NKT cells in various mouse strains

OBJECTIVES: The purpose of this study was to determine whether restrictive left ventricular (LV) filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. BACKGROUND: We recently demonstrated a diastolic ventricular interaction in approximately 50% of a series of patients with chronic heart failure, as evidenced by paradoxic increases in LV end-diastolic volume despite reductions in right ventricular end-diastolic volume during volume unloading achieved by lower body negative pressure (LBNP). We reasoned that such an interaction would impede LV filling in mid and late diastole, but would be minimal in early diastole, resulting in a restrictive LV filling pattern. METHODS: Transmitral flow was assessed using pulsed wave Doppler echocardiography in 30 patients with chronic heart failure and an LV ejection fraction < or = 35%. Peak early (E) and atrial (A) filling velocities and E wave deceleration time were measured. Left ventricular end-diastolic volume was measured using radionuclide ventriculography before and during -30-mm Hg LBNP. RESULTS: Nine of the 11 patients with and 2 of the 16 patients without restrictive LV filling patterns (E/A > 2 or E/A 1 to 2 and E wave deceleration time < or = 140 ms) increased LV end-diastolic volume during LBNP (p = 0.001). The change in LV end-diastolic volume during LBNP was correlated with the baseline A wave velocity (r = -0.52, p = 0.005) and E/A ratio (r = 0.50, p = 0.01). CONCLUSIONS: Restrictive LV filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. Volume unloading in the setting of diastolic ventricular interaction allows for increased LV filling. Identifying patients with chronic heart failure and restrictive filling patterns may therefore indicate a group likely to benefit from additional vasodilator therapy.     

Effects of valve replacement on ventricular mechanics in mitral regurgitation and aortic stenosis

BACKGROUND: This study in humans assessed changes in left ventricular function early and late after correction of mitral regurgitation (MR) (n = 9) or aortic stenosis (AS) (n = 10). METHODS: Ventricular function was measured with radionuclide and micromanometer-derived pressure-volume loops during preload manipulation, thermodilution cardiac outputs, and echocardiograms. Late radionuclide and echocardiographic data were acquired at 24 hours and 20 months. RESULTS: Perioperative left ventricular performance (stroke work-end-diastolic volume relationship) did not change for patients with MR or AS. Significant changes in afterload occurred: ejection fraction (MR, 0.49 to 0.37; AS, 0.54 to 0.60; both, p = 0.013), mean left ventricular ejection pressure (MR, 73 to 91 mm Hg; AS, 138 to 93 mm Hg; both, p < 0.01), and end-systolic wall stress (MR, 26 to 42 x 10(3) dynes/cm2; AS, 37 to 22 x 10(3) dynes/cm2; both, p < 0.01). Ejection efficiency improved for MR patients (0.69 +/- 0.26 to 1.0 +/- 0.15; p < 0.05). The 20-month data showed improved New York Heart Association functional class, normal resting ejection fraction, and normal exercise response for both groups. CONCLUSIONS: Early after operation, a significant change in left ventricular load was seen with correction of MR and AS. Data obtained late after operation showed improvement consistent with ventricular remodeling.     

Isoflurane and halothane do not alter the enhanced afterload sensitivity of left ventricular relaxation in dogs with pacing-induced cardiomyopathy

BACKGROUND: The afterload dependence of left ventricular (LV) relaxation is accentuated in the failing heart. The authors tested the hypothesis that isoflurane and halothane alter the afterload sensitivity of LV relaxation in dogs with pacing-induced cardiomyopathy. METHODS: Dogs (n = 6) were chronically instrumented for measurement of LV and aortic pressures and subendocardial segment length. Hemodynamics were recorded, and LV relaxation was evaluated with a time constant of isovolumic relaxation (tau) under control conditions and during decreases and increases in LV load produced by abrupt inferior vena caval (IVC) occlusion and phenylephrine (intravenous infusion), respectively, in the conscious state and during isoflurane and halothane anesthesia (1.5 MAC) on separate days before and after the development of pacing-induced cardiomyopathy. The slope (R) of the tau versus LV end-systolic pressure (P[es]) relation was also used to determine the afterload sensitivity of LV relaxation. RESULTS: IVC occlusion and phenylephrine produced similar or less profound changes in P(es), regional end-systolic force (an index of LV afterload), and end-systolic segment length in cardiomyopathic compared with healthy dogs. However, IVC occlusion and phenylephrine caused more pronounced alterations in tau in conscious and isoflurane- and halothane-anesthetized dogs after the development of cardiomyopathy. R was also greater in cardiomyopathic compared with healthy dogs (e.g., 0.32 +/- 0.03 before pacing to 1.00 +/- 0.13 ms/mmHg in conscious dogs). No differences in the load dependence of LV relaxation were observed between the conscious and anesthetized states before and after production of LV dysfunction. CONCLUSIONS: The results indicate that isoflurane and halothane do not alter the afterload dependence of LV relaxation in the normal and cardiomyopathic heart. The lack of effect of the volatile anesthetics is probably related to anesthetic-induced reductions in the resistance to LV ejection concomitant with simultaneous negative inotropic effects.     

Immediate reproducibility of upper limit of vulnerability measurements in patients undergoing transvenous implantable cardioverter defibrillator implantation

BACKGROUND: Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early- than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. METHODS AND RESULTS: Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2+/-10.6 to 113+/-16.5 ms acutely and to 133.8+/-25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27+/-15% and 15+/-17%, respectively. The early-activated LV free wall became significantly (17+/-17%) thinner, whereas the late-activated septum thickened significantly (23+/-12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39+/-13%. In paced animals, cardiomyocyte diameter was significantly (18+/-7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. CONCLUSIONS: Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen.     

Verification of accuracy of several algorithms to quantitate left ventricular regional wall motion: a study using cine MR imaging with myocardial tagging

To verify the accuracy of several algorithms used to quantitate left ventricular (LV) regional wall motion, five volunteers were examined by cine MR imaging with presaturation myocardial tagging in short-axis and 4-chamber sections. Three algorithms for the wall motion analysis, radial, centerline, and originally developed "modified-Hildreth" methods, were applied to the cine MR images, and dissociation of the end-systolic position of the tags estimated by each algorithm from the true position was examined. The modified-Hildreth method was comparable in accuracy to the other methods for estimating end-systolic tag position. Significantly worse estimation of the tag position by the three algorithms occurred in the 4-chamber section compared with the short-axis section (p < 0.001, 0.005), indicating difficulties in the wall motion analysis of "long-axis" LV images. Among the algorithms, the centerline method showed the highest accuracy of the estimation in the 4-chamber section, and the modified-Hildreth method was the best in the short-axis section. In the 4-chamber section, correction of the position of end-diastolic and end-systolic images around the luminal centroids improved the estimation (p < 0.01, 0.05). Tagging cine MR imaging was proved to be useful for determining the most suitable algorithm for quantitative wall motion analysis of LV images obtained from conventional angiocardiography and other imaging modalities.     

Echocardiography in the evaluation of ventricular function

The ultrasonic beam used for quantitative assessment of left ventricular (LV) function traverses the heart in a projection similar to the familiar angiographic left anterior oblique projection. It crosses the anterior wall of the right ventricle, the right ventricular cavity, the interventricular septum, the LV cavity and the posterior wall of the left ventricle. Whereas the cyclic changes of the right ventricular diameter are rarely clearly determined by echocardiography, the easily assessed cyclic changes of the LV endocardial transverse diameter are useful measure of LV FUNCTION. Of practical importance are the percentage of systolic shortening of the LV diameter (%Sh) and the mean velocity of circumferential fiber shortening (VCF). There are several factors, such as placing of the ultrasonic transducer, the shape and size of the LV cavity and rotational movements of the heart as a whole, that influence echocardiographic determination of the transverse LV diameter. In patients with asynergic contraction, %Sh and VCF cannot be used as measures of overall LV performance, but localized contraction disturbances of the septum and the posterior wall may be detected from the reduced extent of wall motion in a given LV segment during a full sweep from the base to the apex. The most important indications for echocardiographic assessment of LV function are valvar diseases with chronic LV pressure or volume overload, and congestive cardiomyopathy. Echocardiography has proved useful in serial evaluation of LV function in patients undergoing valvar heart surgery. Assessment of LV volume by standard echocardiography using the cubic formula is not satisfactory. More accurate determination of volumes is provided by formulas that include the actual ratio of the LV long axis to the minor axis.     

Effects of cyclical etidronate therapy on bone loss in early postmenopausal women who are not undergoing hormonal replacement therapy

1. Pacing-induced heart failure was studied in eight dogs. Heart failure was induced by right ventricular pacing at 250-260 beats/min for 6 weeks. Evidence of heart failure was determined clinically and by measurement of left ventricular (LV) dimensions by transoesophageal echocardiography. 2. Haemodynamic measurements of LV pressure, maximum rate of rise of LV pressure (LVdP/dtmax), cardiac output, mean arterial pressure, heart rate, pulmonary artery and pulmonary wedge pressures were made during infusion of solvent (control) and the calcium sensitizer EMD 57033 (0.6 mg min-1 kg-1). 3. The degree of heart failure varied from mild to severe in different individuals, but in each case EMD 57033 exerted a positive inotropic effect on LV haemodynamics and dimension. 4. The positive inotropic effect of the calcium sensitizer was manifest by increased peak LVdP/dt with a subsequent increase in cardiac output at the same mean arterial pressure. 5. This study clearly demonstrates that there is the potential for improvement of contractility of the failing myocardium of the intact mammal by an agent with a mechanism of action which does not involve an increase in intracellular calcium.     

Effect of endurance training on cardiac morphology in Alaskan sled dogs

The cardiac morphology of 77 conscious Alaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied using two-dimensional and M-mode echocardiography. Subgroups included dogs with at least one season of previous training ("veterans") and dogs undergoing their first season of training ("rookies"). Training resulted in a significant (P < 0.05) decrease in resting heart rate (-15%) and significant increases in interventricular septal thickness (systole, 15%; diastole, 13%), left ventricular (LV) internal dimension in diastole (LVIDd, 4%), LV free wall thickness in systole (9%) and diastole (LVWd, 9%), and left atrial diameter (5%) in all dogs, but the increase in LVWd was greater in rookies (16%) than in veterans (7%). Training increased end-diastolic volume index (8%), LV mass index (24%), and heart weight index (24%) and decreased the LVIDd-to-LVWd ratio (-6%) but did not alter cardiac index. We conclude that increased LV mass attributable to LV dilation and hypertrophy is associated with endurance training in Alaskan sled dogs. Disproportionate LV wall thickening accompanying LV dilation suggests that cardiac morphological changes are due to volume and pressure loading. These training-induced changes are similar to those documented in human athletes undergoing combined isometric and isotonic training and differ from studies of dogs trained on treadmills.     

Application of mechanical restitution: variation of inotropic effects of vagal stimulation or verapamil administration during irregular cardiac rhythm

The effects of verapamil administration or vagal stimulation on the mechanical restitution curve (MRC) were studied in order to better understand the modulation of left ventricular (LV) function by interventions that lower the ventricular rate of atrial fibrillation. The MRC and the postextrasystolic MRC were obtained in 11 dogs using peak single beat elastance (Emax). The MRC was fitted by a monoexponential curve. Vagal stimulation or verapamil administration decreased the peak of the MRC and right-shifted the MRC. The postextrasystolic MRC was located upward compared with the control MRC, and was shifted downward by vagal stimulation or verapamil administration. If interventions having a negative inotropic effect effectively slow a rapid heart rate, the net effect of the ventricular contractile state may not always be negative. It was concluded that the MRC is useful in understanding LV contractility during irregular rhythm, especially when assessing the net effect of the negative dromotropic and inotropic action of antiarrhythmic drugs.     

Cardiomyoplasty: hemodynamic benefit to normal and depressed canine left ventricular function

This study examined the effects of cardiomyoplasty with vascular delay on canine normal and depressed left ventricular (LV) function. To improve viability of the latissimus dorsi muscle (LDM), vascular delay was performed 2 weeks before cardiomyoplasty in 10 mongrel dogs. Two weeks after cardiomyoplasty, LV function was evaluated by simultaneously measuring LV and aortic pressure, and aortic flow. The LDM was stimulated at a ratio of 1:4-1:7 synchronously with ventricular systole. Microspheres (90 mu) were sequentially injected into the left coronary artery to depress LV function. Data were acquired and analyzed on a beat to beat basis. Results were as follows: LDM stimulation significantly augmented LV systolic pressure (LVSP) from 138 +/- 2 to 161 +/- 2* mmHg, the peak rate of change of LV pressure (+dP/dt) from 1888 +/- 46 to 2584 +/- 43* mmHg/sec, aortic systolic pressure (AoSP) from 140 +/- 2 to 159 +/- 2* mmHg, stroke volume (SV) from 11.2 +/- 0.3 to 13.3 +/- 0.3* ml, stroke work (SW) from 19 +/- 1 to 26 +/- 1* gm.m, peak aortic flow (P Qa) from 5542 +/- 142 to 7190 +/- 161* ml/min, and decreased -dP/dt from -1683 +/- 31 to -1689 +/- 49* mmHg/sec (* = p < 0.05). Microsphere injections depressed LV function, but did not affect the magnitude of the net changes between stimulated and nonstimulated beats. However, the percent changes significantly increased. Preconditioning of LDM with vascular delay augments cardiac function in LDM assisted beats. This improved performance was present in both normal as well as depressed LV function groups. Thus, investigations of cardiomyoplasty may not necessarily require a model of severe myocardial dysfunction. Vascular delay offers an important preconditioning method of LDM to augment cardiac function in cardiomyoplasty.     

Cardiac sympathetic stimulation increases cardiac contractility but decreases contractile efficiency in canine hearts in vivo

The effect of cardiac sympathetic stimulation on cardiac contractile efficiency was studied in dogs. In 19 anesthetized and open-chest dogs, left ventricular (LV) pressure, LV volume, coronary blood flow and coronary venous oxygen saturation were measured simultaneously. The LV end-systolic pressure volume relations (ESPVR) and the relation between myocardial oxygen consumption (VO2)-pressure volume area (PVA) were obtained during a transient occlusion of the inferior vena cava before and after sympathetic stimulation (9V, 6 Hz, 40 sec) both with and without 50 mg/kg of 2,3-butanedione monoxime (BDM). Without BDM, sympathetic stimulation increased the slope of ESPVR by 62% (p<0.05), the slope of the VO2-PVA line by 19% (p<0.05) and the y-axis intercept of the VO2-PVA by 65% (p<0.05). With BDM, the increase in the slope of the VO2-PVA line became insignificant although other responses were similarly preserved. These data imply that cardiac sympathetic stimulation decreases cardiac contractile efficiency through mechanisms by which norepinephrine-induced beta-adrenergic activation enhances myosin ATPase-operating ATP hydrolysis in crossbridge formation.     

Influence of heart rate on stroke volume variability in atrial fibrillation in patients with normal and impaired left ventricular function

Both resting tachycardia and irregular ventricular rhythm may contribute to impaired cardiac performance in atrial fibrillation (AF). This study assesses the relation between resting heart rate and beat-to-beat changes in left ventricular (LV) ejection and filling in patients with normal and impaired LV systolic function. Beat-to-beat variation in LV outflow and inflow velocity-time integral was measured using pulsed Doppler ultrasound in 39 patients with chronic AF and normal (n=22) or impaired (n=17) LV systolic function. Aortic velocity-time integral variability increased with mean heart rate (p=0.003) even though RR interval variability decreased (p <0.001). Aortic velocity-time integral was more sensitive to the duration of both the preceding (p <0.001) and prepreceding (p <0.001) RR intervals at higher heart rates. These relations were similar for patients with normal and impaired LV systolic function. The sensitivity of the filling velocity-time integral to RR interval variability also increased with heart rate (p <0.001). However, at higher heart rates the filling velocity-time integral (p=0.009) and filling time (p=0.005) were less sensitive to change in RR intervals in patients with impaired LV function. We conclude that beat-to-beat stroke volume variability in AF increases with heart rate. Stroke volume variability was not influenced by LV systolic function.     

Patterns of grief reaction after pregnancy loss

BACKGROUND: Different regions within the left ventricle are preferentially supplied by the left or right sympathetic system. In order to characterize different influences of left vs right sympathetic lateralization on LV function, haemodynamic effects of right and left stellate ganglion stimulations (RSGS and LSGS) as well as a right sympathetic block (RSB) were compared. METHODS: Seven alpha-chloralose anaesthetized open chest dogs were instrumented for measurement of LV pressure (tip manometers) and regional LV wall thickness (WT, sonomicrometry) in the antero-apical wall (AW, innervated by right stellate ganglion) and postero-basal wall (PW, left stellate ganglion). Timing of regional myocadial wall motion was evaluated by the phase of the first Fourier transform of the WT signals, LV asynchrony by the phase difference (phi) between both regions, and LV diastolic function by the time constant of isovolumic relaxation (tau). Measurements were performed before and after RSB (5 ml of lidocaine 1%); in 6 dogs of this group, RSGS and LSGS (4 V, 0.2 ms, 20 Hz) were performed before RSB. In order to investigate a regional inotropic stimulation without systemic effect, 6 additional dogs received intracoronary noradrenaline injections (NIC, 0.25 microgram) into the left circumflex artery perfused myocardium. RESULTS: LSGS and NIC led to an earlier PW-motion within the cardiac cycle (phase reduction by 40.0 +/- 15.0 degree (SEM) and 55.5 +/- 11.2 degrees) and RSGS induced an earlier AW-motion (by 33.7 +/- 15.2 degrees). After RSB, AW-motion was delayed (38.1 +/- 9.2 degrees). The consequence was an asynchronous wall motion pattern after all interventions (change in phi: LSGS-64.7 +/- 18.7 degrees, RSGS 41.1 +/- 15.7 degrees, NIC -74.5 +/- 17.4 degrees, RSB -52.6 +/- 14.6 degrees), and a prolonged relaxation (tau increase: RSGS 9.4 +/- 1.9, NIC 8.3 +/- 1.5, RSB 3.7 +/- 0.8 ms). CONCLUSION: Unilateral increases as well as decreases of sympathetic tone to the heart result in an asynchronous wall motion pattern and an impaired LV relaxation.