Effects of partial left ventriculectomy on left ventricular performance in patients with nonischemic dilated cardiomyopathy

Objectives. This study sought to assess the effects of partial left ventriculectomy (PLV) on left ventricular (LV) performance in a series of consecutive patients with nonischemic dilated cardiomyopathy.

Background. Reduction of LV systolic function in patients with heart failure is associated with an increase of LV volume and alteration of its shape. Recently, PLV, a novel surgical procedure, was proposed as a treatment option to alter this process in patients with dilated cardiomyopathy.

Methods. We studied 19 patients with severely symptomatic nonischemic dilated cardiomyopathy, before and 13 ± 3 days after surgery, and 12 controls. Single-plane left ventriculography with simultaneous measurements of femoral artery pressure was performed during right heart pacing.

Results. The LV end-diastolic and end-systolic volume indexes decreased after PLV (from 169 to 102 ml/m², and from 127 to 60 ml/m², respectively, p < 0.0001 for both). Despite a decrease in LV mass index (from 162 to 137 g/m², p < 0.0001), there was a significant decrease in LV circumferential end-systolic and end-diastolic stresses (from 277 to 159 g/cm², p < 0.0001 and from 79 to 39 g/cm², p = 0.0014, respectively). Ejection fraction improved (from 24% to 41%, p < 0.0001); the stroke work index remained unchanged.

Conclusions. The PLV improves LV performance by a dramatic reduction of ventricular end-systolic and end-diastolic stresses. Further studies are needed to assess whether this effect is sustained during long-term follow-up and to define the role of PLV in the treatment of patients with dilated cardiomyopathy.     

Results of partial left ventriculectomy for dilated cardiomyopathy: hemodynamic, clinical and echocardiographic observations

OBJECTIVES

The study was done to prospectively measure the echocardiographic, hemodynamic and clinical outcomes after partial left ventriculectomy (PLV).

BACKGROUND

Although PLV can improve symptoms of advanced heart failure, immediate postoperative echocardiographic findings remain abnormal.

METHODS

Fifty-nine patients with cardiomyopathy and advanced heart failure underwent PLV and concomitant mitral valve surgery between May 1996 and December 1997. Thirty-nine percent were on inotropic therapy. All were New York Heart Association (NYHA) functional class III or IV. Mechanical circulatory support (LVAD) and transplant were provided for rescue therapy when hemodynamic compromise occurred. Patients were followed for a mean of 405 ± 168 days, and clinical, echocardiographic and hemodynamic measures were obtained preoperatively, immediately postoperatively, and at 3 and 12 months prospectively.

RESULTS

Comparing preoperative and 12-month postoperative values in event-free survivors, we found: NYHA functional class improved from 3.6 to 2.1, p < 0.0001; peak oxygen consumption increased from 10.8 to 16.0 ml/kg/min, p < 0.0001; LV ejection fraction increased from 13 ± 6.0% to 24 ± 6.9%, p < 0.0001; LV end diastolic diameter decreased from 8.2 ± 1.03 to 6.2 ± 0.64 cm, p < 0.0001, and volume was reduced from 167 ± 60 to 105 ± 38 ml/m², P = 0.02. Central hemodynamics did not normalize after surgery.

CONCLUSIONS

Partial left ventriculectomy can provide structural remodeling of the heart that may result in temporary improvement in clinical compensation. However, perioperative failures and the return of heart failure limit the propriety of this procedure.     

Long-term effects of carvedilol in idiopathic dilated cardiomyopathy with persistent left ventricular dysfunction despite chronic metoprolol

OBJECTIVES

The purpose of this study was to analyze whether long-term treatment with the nonselective beta-adrenergic blocking agent carvedilol may have beneficial effects in patients with dilated cardiomyopathy (DCM), who are poor responders in terms of left ventricular (LV) function and exercise tolerance to chronic treatment with the selective beta-blocker metoprolol.

BACKGROUND

Although metoprolol has been proven to be beneficial in the majority of patients with heart failure, a subset of the remaining patients shows long-term survival without satisfactory clinical improvement.

METHODS

Thirty consecutive DCM patients with persistent LV dysfunction (ejection fraction ≤40%) and reduced exercise tolerance (peak oxygen consumption <25 ml/kg/min) despite chronic (>1 year) tailored treatment with metoprolol and angiotensin-converting enzyme inhibitors were enrolled in a 12-month, open-label, parallel trial and were randomized either to continue on metoprolol (n = 16, mean dosage 142 ± 44 mg/day) or to cross over to maximum tolerated dosage of carvedilol (n = 14, mean dosage 74 ± 23 mg/day).

RESULTS

At 12 months, patients on carvedilol, compared with those continuing on metoprolol, showed a decrease in LV dimensions (end-diastolic volume −8 ± 7 vs. +7 ± 6 ml/m², p = 0.053; end-systolic volume −7 ± 5 vs. +6 ± 4 ml/m², p = 0.047), an improvement in LV ejection fraction (+7 ± 3% vs. −1 ± 2%, p = 0.045), a reduction in ventricular ectopic beats (−12 ± 9 vs. +62 ± 50 n/h, p = 0.05) and couplets (−0.5 ± 0.4 vs. +1.5 ± 0.6 n/h, p = 0.048), no significant benefit on symptoms and quality of life and a negative effect on peak oxygen consumption (−0.6 ± 0.6 vs. +1.3 ± 0.5 ml/kg/min, p = 0.03).

CONCLUSIONS

In DCM patients who were poor responders to chronic metoprolol, carvedilol treatment was associated with favorable effects on LV systolic function and remodeling as well as on ventricular arrhythmias, whereas it had a negative effect on peak oxygen consumption.     

Transmural contractile reserve after reperfused myocardial infarction in dogs

OBJECTIVES

The goal of this study was to characterize detailed transmural left ventricular (LV) function at rest and during dobutamine stimulation in subendocardial and transmural experimental infarcts.

BACKGROUND

The relation between segmental LV function and the transmural extent of myocardial necrosis is complex. However, its detailed understanding is crucial for the diagnosis of myocardial viability as assessed by inotropic stimulation.

METHODS

Short-axis tagged magnetic resonance images were acquired at five to seven levels encompassing the LV from base to apex in seven dogs 2 days after a 90-min closed-chest left anterior descending coronary occlusion, followed by reflow. Myocardial strains were measured transmurally in the entire LV by harmonic phase imaging at rest and 5 ig.kg⁻¹.min⁻¹ dobutamine. Risk regions were assessed by radioactive microspheres, and the transmural extent of the infarct was assessed by 2,3,5 triphenyltetrazolium chloride staining.

RESULTS

Circumferential shortening (Ecc), radial thickening (Err) and maximal shortening at rest were greater in segments with subendocardial versus transmural infarcts, both in subepicardium (−1.1 ± 1.0 vs. 2.5 ± 0.6% for Ecc, −0.5 ± 1.9 vs. −1.8 ± 1.0% for Err, p < 0.05) and subendocardium (−2.0 ± 1.4 vs. 2.8 ± 0.8%, 2.4 ± 1.7 vs. 0.0 ± 0.9%, respectively, p < 0.05). Under inotropic stimulation, risk regions retained maximal contractile reserve. Recruitable deformation was found in outer layers of subendocardial infarcts (p < 0.01 for Ecc and Err) but also in inner layers (p < 0.01). Conversely, no contractile reserve was observed in segments with transmural infarcts.

CONCLUSIONS

Under dobutamine challenge, recruitment of myofiber shortening and thickening was observed in inner layers of segments with subendocardial infarcts. These results may have important clinical implications for the detection of myocardial viability.     

Effect of very early angiotensin-converting enzyme inhibition on left ventricular dilation after myocardial infarction in patients receiving thrombolysis: results of a meta-analysis of 845 patients. FAMIS, CAPTIN and CATS Investigators

OBJECTIVES

We sought to investigate the effect of angiotensin-converting enzyme (ACE) inhibition <9 h after myocardial infarction (MI) on left ventricular (LV) dilation in patients receiving thrombolysis.

BACKGROUND

The ACE inhibitors reduce mortality after MI. Attenuation of LV dilation has been suggested as an important mechanism.

METHODS

The data of 845 patients with three-month echocardiographic follow-up after MI were combined from three randomized, double-blind, placebo-controlled studies. The criteria for these studies included: 1) thrombolytic therapy; 2) ACE inhibition within 6 to 9 h; and 3) evaluation of LV dilation as the primary objective.

RESULTS

The ACE inhibitor was started 3.2 ± 1.7 h after the patients’ first (mainly, 85%) anterior MI. After three months, LV dilation was not significantly attenuated by very early treatment with an ACE inhibitor. The diastolic volume index was attenuated by 0.5 ml/m² (95% confidence interval [CI] −1.5 to 2.5, P = 0.61), and the systolic volume index by 0.5 ml/m² (95% CI −1.0 to 1.9, P = 0.50). Subgroup analysis demonstrated that LV dilation was significantly attenuated by ACE inhibitor treatment for patients in whom reperfusion failed. In contrast, LV dilation was almost unaffected by ACE inhibitor treatment in successfully reperfused patients.

CONCLUSIONS

We could not demonstrate attenuation of LV dilation in patients receiving thrombolysis by ACE inhibitor treatment within 6 to 9 h after MI. We speculate that very early treatment with an ACE inhibitor has a beneficial effect on LV remodeling only in patients in whom reperfusion failed. Other mechanisms may be responsible for the beneficial effects of ACE inhibitors in successfully reperfused patients after MI.     

Dissociation Between Changes in Intramyocardial Function and Left Ventricular Volumes in the Eight Weeks After First Anterior Myocardial Infarction

Objectives. We sought to examine the relation between regional changes in intramyocardial function and global left ventricular (LV) remodeling in the first 8 weeks after reperfused first anterior myocardial infarction (MI).

Background. Because of limitations in imaging methods used to date, this relation has not been thoroughly evaluated.

Methods. We studied 26 patients (21 men, 5 women; mean age 51 years) by magnetic resonance imaging (MRI) on day 5 ± 2 (mean ± SD) and week 8 ± 1 after their first anterior MI. All patients had single-vessel left anterior descending coronary artery disease and although they had received reperfusion therapy, all had regional LV dysfunction and an initial ejection fraction (EF) ≤50%. Short-axis magnetic resonance tagging was performed spanning the LV. Percent intramyocardial circumferential shortening (%S) on a topographic basis, LV mass index, LV end-diastolic volume index (LVEDVI), LV end-systolic volume index and LV ejection fraction (LVEF) were measured.

Results. Left ventricular mass index tended to decrease, whereas the LVEDVI increased from 82 ± 24 to 96 ± 27 ml/m² (p = 0.002). Left ventricular end-systolic volume index remained unchanged, whereas LVEF increased from 39 ± 12% to 45 ± 14% (p = 0.002). Apical %S improved from 9 ± 6% to 13 ± 5% (p < 0.0001), as it did in the midanterior (6 ± 6% to 10 ± 7%, p < 0.02) and midseptal regions (8 ± 7% to 12 ± 6%, p < 0.02). Early dysfunction in remote midinferior and basal lateral regions resolved by 8 weeks. By multivariate analysis, the only significant predictor of an increase in LVEDVI over the study period was peak creatine kinase (p = 0.04).

Conclusions. In the first 8 weeks after a large, reperfused anterior MI, %S improved in the apex, midanterior and midseptal regions and normalized in remote noninfarct-related regions, but LV end-diastolic volumes also increased. This increased LVEDVI correlated with infarct size by peak creatine kinase and was not related to changes in global and regional LV function.     

R013-6438, a new inotrope-vasodilator: Systemic and coronary hemodynamic effects in congestive heart failure

Systemic and coronary hemodynamics and transmyocardial norepinephrine release were determined before and after oral administration of RO13-6438, a new inotrope-vasodilator agent, in 12 patients with severe chronic heart failure unresponsive to conventional and vasodilator therapy. improvement in left ventricular (LV) function was evident from a marked increase in cardiac index (from 2.09 ± 0.45 to 3.30 ± 0.73 liters/min/m2, p <0.01), stroke volume index (from 23 ± 7 to 36 ± 11 ml/m2, p <0.01), and stroke work index (from 23 ± 11 to 36 ± 14 g-m/m², p <0.01), and concomitant fall in pulmonary capillary wedge pressure (from 26 ± 7 to 16 ± 8 mm Hg, p <0.01). Myocardial oxygen consumption did not change significantly (from 15.3 ± 6.8 to 14.9 ± 6.8 mi/min), but the ratio of minute work/myocardial oxygen consumption, an index of LV efficiency, Increased significantly (p <0.05). Although average coronary sinus flow did not change, coronary sinus oxygen increased (from 3.2 ± 0.8 to 4.2 ± 1.5 vol%, p <0.05), and arterial-coronary sinus oxygen difference decreased (from 11.8 ± 2.1 to 10.4 ± 1.9 vol%, p <0.05), suggesting a primary vasodilating effect of R013-6438 on the coronary vascular bed. Net transmyocardial norepinephrine release did not change despite the marked hemodynamic improvement. These findings suggest that R013-6438 has the potential to cause marked improvement in LV function and LV efficiency in patients with severe, refractory congestive heart failure.     

Left ventricular diastolic function in weight lifters

Concentric left ventricular (LV) hypertrophy and asymmetric septal hypertrophy have both been described in weight lifters, but diastolic filling, which is abnormal in pathologically hypertrophied ventricles, has not been investigated in such subjects. Accordingly, pulsed Doppler examination of LV inflow, M-mode and 2-dimensional echocardiography were performed in 16 competitive weight lifters and 10 age-matched male control subjects. Peak and mean filling rates were determined in milliliters per second as the product of the cross-sectional area of the mitral anulus and the Doppler-derived peak early and mean transmitral inflow velocities, respectively. Rapid filling index was defined as peak filling rate divided by mean filling rate. Flow velocity integrals of the early and atrial diastolic filling phases were also measured. LV end-diastolic volume and ejection fraction were measured using 2-dimensional echocardiography. Weight lifters had significantly higher LV end-diastolic volume (181 ± 50 vs 136 ± 40 ml, p < 0.05) and dimension (5.6 ± 0.6 vs 5.1 ± 0.5 cm, p < 0.05), and posterior wall thickness (0.9 ± 0.2 vs 0.8 ± 0.1, p < 0.05); however, after correction for body surface area there was no significant difference in these values. Weight lifters had significantly higher LV mass (241 ± 70 vs 165 ± 29, p < 0.02) and LV mass index (114 ± 29 vs 87 ± 15 g/m², p < 0.05). There was no significant difference between the weight lifters and control subjects in rapid filling index, early to late integral ratio or ejection fraction. Five of the weight lifters competed nationally and took steroids heavily; in this group diastolic function was abnormal. Thus, weight lifters have concentric LV hypertrophy but normal diastolic function, consistent with physiologic hypertrophy.     

Effects of intravenous administration of nicorandil on cardiovascular hemodynamics and left ventricular function

The effects of the intravenous administration of the antianginal drug, nicorandil, 50 μg/kg administered over 2 minutes, were investigated during pacing-induced ischemia in 8 patients with coronary artery disease. Hemodynamic parameters were measured and single-plane left ventriculograms were obtained in control and postpacing periods both before and after pretreatment with nicorandil. Regional wall motion of the left ventricle was assessed by measuring shortening of the radial axes originating from the center of gravity of the end-diastolic silhouette. Heart rate, left ventricular (LV) systolic pressure and end-diastolic volume index did not change in the immediate postpacing period with or without medication. LV end-diastolic pressure decreased with nicorandil, from 22.0 ± 3.4 to 17.0 ± 2.3 mm Hg (mean ± standard error of the mean) (p < 0.05), and LV systolic volume index, from 39.6 ± 8.0 to 30.4 ± 6.8 ml/m² (p < 0.05). Ejection fraction increased from 55.2 ± 5.0 to 64.3 ± 3.8% (p < 0.05). Stroke index and cardiac index (calculated from heart rate and stroke index) did not change significantly. Rapid right ventricular pacing increased the extent and degree of dyskinesia of the left ventricle, but premedication with nicorandil improved the wall motion. Thus, nicorandil has salutary effects on ventricular contractile and hemodynamic responses to transient ischemia induced by pacing stress.     

Comparison of time of reperfusion during anterior wall acute myocardial infarction to left ventricular volume one month and 20 months later

We studied 95 patients with a first anterior wall acute myocardial infarction who received successful reperfusion within 72 hours after the onset. The patients were divided into 4 groups based on the time required to achieve reperfusion; <3 hours (n = 23), 3 to 6 hours (n = 42), 6 to 24 hours (n = 17), and >24 to 72 hours (n = 13). The infarct size, as evaluated by thallium-201 single-photon emission computed tomography, at 1 month after the infarct was significantly larger (p <0.05) in >24 to 72 hours (1,593 ± 652 U) than that in <3 hours (749 ± 650 U), but was not significantly different from that at 3 to 6 hours (1,353 ± 770 U) or 6 to 24 hours (1,371 ± 561 U). The end-diastolic volume index at 1 month did not differ among the 4 groups. However, the end-diastolic volume index during the follow-up period (20 ± 8 months) in >24 to 72 hours (93 ± 23 ml/m²) was significantly larger than that in the other 3 groups (<3 hours [65 ± 21 ml/m²], 3 to 6 hours [65 ± 22 ml/m²], and 6 to 24 hours [70 ± 25 ml/m²]). Similar findings were observed in end-systolic volume index. In conclusion, although infarct size reduction was not observed by late reperfusion, left ventricular volumes at 1 month were comparable among patients with successful reperfusion within 3 and up to >24 hours. Left ventricular volumes 2 years after acute myocardial infarction were significantly larger in patients who did not under reperfusion for >24 hours.     

Coronary flow velocity immediately after primary coronary stenting as a predictor of ventricular wall motion recovery in acute myocardial infarction

OBJECTIVES

The purpose of this study was to examine the relationship between the pattern of coronary blood flow velocity immediately after successful primary stenting and the recovery of left ventricular (LV) wall motion in patients with acute myocardial infarction (AMI).

BACKGROUND

It is difficult to predict the recovery of LV wall motion immediately after direct angioplasty in AMI. Recent reports indicate that dysfunctional coronary microcirculation is an important determinant of prognosis for AMI patients after successful reperfusion.

METHODS

We measured left anterior descending coronary flow velocity variables using a Doppler guide wire immediately after successful primary stenting in 31 patients with their first anterior AMI. The patients were divided into two groups: those with and those without early systolic reverse flow (ESRF). Changes in LV regional wall motion (RWM) and ejection fraction (EF) at admission and at discharge were compared between the two groups. Coronary flow velocity variables immediately after primary stenting were compared with changes in left ventriculographic indexes.

RESULTS

The change in RWM was significantly greater in the non-ESRF group than it was in the ESRF group (0.9 ± 0.7 vs. −0.1 ± 0.3 standard deviation/chord, respectively, p < 0.001). The change in EF was also significantly greater in the non-ESRF group than it was in the ESRF group (10 ± 10 vs. 1 ± 6%, respectively, p < 0.05). In the non-ESRF group (diastolic to systolic velocity ratio [DSVR] <3.0), the DSVR correlated positively with the change in RWM (r = 0.60, p < 0.005, n = 24) and the change in EF (r = 0.52, p < 0.01).

CONCLUSIONS

The coronary flow velocity pattern measured immediately after successful primary stenting is predictive of the recovery of regional and global LV function in patients with AMI.     

Abnormal cardiac function in the streptozotocin-induced non-insulin-dependent diabetic rat: noninvasive assessment with doppler echocardiography and contribution of the nitric oxide pathway

OBJECTIVES

We sought to evaluate in vivo and in vitro left ventricular (LV) geometry and function in streptozotocin-induced diabetic rats and the possible role of the nitric oxide (NO) pathway.

BACKGROUND

Diabetes results in cardiac dysfunction; however, the specific abnormalities are unknown. Because decreased NO contributes to abnormal vascular function in diabetics, we hypothesized that NO pathway abnormalities may contribute to diabetic cardiomyopathy.

METHODS

Control rats and those with non–insulin-dependent diabetes mellitus (NIDDM) underwent echocardiography, hemodynamic assessment, isolated heart perfusion and measurement of exhaled NO and LV endothelial constitutive nitric oxide synthase (ecNOS).

RESULTS

Diabetic rats had increased LV mass (3.3 ± 0.6 vs. 2.6 ± 0.3 g/g body weight [BW], p < 0.001) and cavity dimensions (diastolic 2.0 ± 0.1 vs. 1.8 ± 0.2 cm/cm tibial length [TL], p < 0.05). Diabetic rats had prolonged isovolumic relaxation time (IVRT) (40 ± 8 vs. 26 ± 6 ms, p < 0.0001), increased atrial contribution to diastolic filling (0.47 ± 0.09 vs. 0.30 ± 0.08 m/s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 ± 6 vs. 2 ± 1 mm Hg, p = 0.04). Diabetic rats had increased chamber stiffness. Shortening was similar in both groups, despite reduced meridional wall stress in diabetics, suggesting impaired systolic contractility. Exhaled NO was lower in diabetic rats (1.8 ± 0.2 vs. 3.3 ± 0.3 parts per billion, p < 0.01) and correlated with Doppler LV filling. The ecNOS was similar between the groups.

CONCLUSIONS

Diabetic cardiomyopathy is characterized by LV systolic and diastolic dysfunction, the latter correlating with decreased exhaled NO. The NO pathway is intact, suggesting impaired availability of NO as contributor to cardiomyopathy.     

Tetralogy of fallot with diminutive pulmonary arteries: Preoperative pulmonary valve dilation and transcatheter rehabilitation of pulmonary arteries

Objectives. The study sought to determine the results of a novel transcatheter management approach in tetralogy of Fallot with diminutive pulmonary arteries.

Background. Tetralogy of Fallot with diminutive pulmonary arteries and severe pulmonary stenosis is rare and resembles tetralogy of Fallot with pulmonary stresia: There is a high incidence of aortopulmonary collateral channels, arborization abnormalities, stenoses and need for multiple operations. Because a combined catheter-surgery approach facilitates repair in these patients, such an approach may benefit those with diminative pulmonary arteries and pulmonary stenosis.

Methods. Clinical, catheterization and surgical data were studied retrospectively for 10 such patients undergoing preoperative pulmonary valve balloon dilation, among other transcatheter interventions, from January 1989 to January 1995.

Results. Initially, the Nakata index ranged from 20 to 98 mm²/m² (mean 67 ± 28 mm²/m²). The pulmonary valve was first balloon dilated (mean balloon/annulus 1.5 ± 0.3), and the mean initial valve annulus Z score (−40 ± 1) increased to −3.3 ± 1.1 (p < 0.01). Other interventions included branch pulmonary artery balloon dilation (7 patients, 23 vessels) and coil embolization of aortopulmonary collateral channels (8 patients, 31 collateral channels). At preoperative follow-up catheterization, the mean pulmonary annulus Z score was −3.1 ± 0.7, and the aorta index increased to 143 ± 84 mm²/m² (p < 0.03). All patients underwent complete surgical repair successfully. At a mean follow-up period of 2.6 ± 2 years, right ventricular pressure was < 70% systemic in all patients and <50% systemic in seven.

Conclusions. In patients with tetralogy of Fallot, severe pulmonary stenosis and diminutive pulmonary arteries, initial pulmonary valve balloon dilation increases the annulus Z score and anterograde pulmonary blood flow and facilitates simultaneous coiling of sertopulmonary collateral channels and access for branch pulmonary artery dilation, all of which results in pulmonary artery growth, simpligying surgical management.     

Restricted coronary flow reserve in patients with mitral regurgitation improves after mitral reconstructive surgery

Objectives. The purpose of this study was to assess coronary flow characteristics in patients with chronic mitral regurgitation (MR).

Background. Coronary flow reserve (CFR) has been reported to be restricted in cases with left ventricular (LV) volume overload caused by aortic regurgitation and increased LV preload.

Methods. The study populations consisted of 31 patients with nonrheumatic chronic MR. Eleven with chest pain and normal coronary arteries served as control subjects. Phasic coronary flow velocities were obtained in the proximal segment of the angiographically normal left anterior descending coronary artery at rest and during hyperemia (0.14 mg/kg/min adenosine infusion intravenously) using a 0.014-in. (0.036 cm), 15-MHz Doppler guide wire. Coronary flow reserve was obtained from the ratio of hyperemic/baseline time-averaged peak velocity (APV). Thirteen cases who underwent mitral valve reconstructive surgery were also studied 1 month after surgery.

Results. Compared with control subjects, CFR was significantly reduced in cases with MR (2.1 ± 0.5 vs. 3.3 ± 0.6, respectively, p < 0.01) because baseline APV was significantly greater (28 ± 8 vs. 19 ± 6 cm/s, respectively, p < 0.01), although maximal hyperemic APV was not significantly different (56 ± 14 vs. 61 ± 16 cm/s, respectively, p = NS). Significant correlations were obtained between CFR and LV end-diastolic pressure (LVEDP) (r = 0.70, p < 0.01), LV mass index (r = 0.42, p < 0.01), LV end-diastolic volume (r = 0.38, p = 0.04) and MR volume (r = 0.39, p = 0.03), and stepwise regression analysis showed LVEDP was the most important determinant of CFR in MR (r² = 0.49, p < 0.0001). This restricted CFR improved significantly after mitral valve reconstructive surgery (2.1 ± 0.5 vs. 3.1 ± 0.6, respectively, p < 0.01) because of reduction of baseline APV (28 ± 8 vs. 21 ± 8 cm/s, respectively, p < 0.01).

Conclusions. Coronary flow reserve is limited in cases with MR because of elevation of baseline resting flow velocity. This reduction of CFR correlates well with increase in LV preload, mass and volume overload, especially with increase in LV preload, and this restricted CFR improves after mitral valve surgery.     

Intracoronary prostaglandin E1 plus streptokinase in acute myocardial infarction

Fourteen patients with acute myocardial infarction (duration of chest pain 5 ± 2 hours) received intracoronary infusion of prostaglandin E₁ (PGE₁) and streptokinase. Intracoronary PGE₁ was followed by intracoronary streptokinase in 10 patients (group A), with successful recanalization in all patients. Of 4 patients in whom recanalization failed with intracoronary streptokinase given first (group B), 2 had successful recanalization after addition of intracoronary PGE₁. Immediately after successful recanalization, left ventricular ejection fraction increased from 50 ± 9% to 62 ± 10% (p < 0.0008), left ventricular end-diastolic pressure decreased from 20 ± 10 to 16 ± 10 mm Hg (p < 0.05) and stroke volume index increased from 34 ± 10 to 44 ± 12 ml/m² (p < 0.02). Infarct segment shortening improved from 9 ± 5 to 18 ± 4% (p < 0.0002). Transient hypotension in 1 patient was the only complication. Follow-up catheterization in recanalized patients at 2 to 10 days showed maintained improvement in left ventricular global and infarct segment function. Reocclusion occurred in 1 patient. Thus, intracoronary infusion of PGE₁ was effective in establishing reperfusion in all patients when followed by streptokinase and was associated with immediately improved left ventricular global and regional function. PGE₁ deserves further evaluation in acute myocardial infarction.     

Left ventricular dysfunction after long-term right ventricular apical pacing in the young

OBJECTIVES

The goal of this study was to assess long-term global left ventricular (LV) function in patients paced from the right ventricular (RV) apex at a young age.

BACKGROUND

Ventricular contraction asynchrony with short-term RV apical pacing has been associated with reduced LV pump function and relaxation. The long-term effect of RV apical pacing on global LV function in the young remains unknown.

METHODS

Twenty-four patients with normal segmental anatomy paced from the RV apex (follow-up 1 to 19 years) underwent noninvasive assessment of global LV function with automated border detection echocardiography-derived fractional area of change (FAC), coupled with the Doppler index of myocardial performance (MPI). Data were analyzed from 24 RV-paced patients (mean follow-up 9.5 years, age 19 years, body surface area [BSA] 1.6 m², QRS duration 140 ms) and compared with 33 age- and BSA-matched control subjects (age 16.4 years, BSA 1.6 m²). Multiple linear regression analysis was performed to identify patient variables that can affect these indexes of LV function.

RESULTS

Assessment of LV function (median follow-up 10 years) in 24 paced patients demonstrated impaired area- and Doppler flow-derived indexes of LV systolic and diastolic function, compared with those indexes of control subjects (FAC: 52% vs. 60%, p < 0.01; MPI: 0.46 vs. 0.34, p < 0.01). Paced QRS interval and age were found to significantly influence global LV contraction in these patients (R² = 0.4, p < 0.05).

CONCLUSIONS

In the presence of impaired LV function with long-term RV apical pacing, alternative sites of ventricular pacing that simulate normal biventricular electrical activation should be explored to preserve function in pediatric patients in need of long-term pacing.     

Coronary dilatory capacity in idiopathic dilated cardiomyopathy: Analysis of 16 patients

Hemodynamic function and overall coronary blood flow (argon technique) were measured in 16 patients with idiopathic dilated cardiomyopathy (IDC) and in 12 patients without detectable heart disease (control subjects) referred for precordial pain. In patients with IDC, coronary blood flow was normal at rest (78 ± 17 ml/100 g·min versus 78 ± 9 in control subjects). During maximal inducible coronary vasodilation (dipyridamole, 0.5 mg/kg), coronary blood flow was significantly reduced (142 ± 38 ml/100 g · min versus 301 ± 64 in control subjects; p < 0.001). Consequently, obtainable minimal coronary resistance was increased in IDC (0.54 ± 0.20 mm Hg/ml/100 g · min versus 0.23 ± 0.04 in control subjects; p < 0.001). In patients with IDC, left ventricular (LV) end-diastolic pressure was significantly increased (19 ± 11 mm Hg versus 6 ± 3 in control subjects; p < 0.005), and the LV ejection fraction was diminished (36 ± 11% versus 72 ± 3% in control subjects; p < 0.001). In patients with IDC, LV end-diastolic pressure correlated significantly with the obtained minimal coronary resistance after application of dipyridamole (r = 0.85; p < 0.001). LV catheter biopsy specimens revealed no alterations in myocardial microvasculature. Thus, coronary dilatory capacity is impaired in patients with IDC, due partially to an increase in extravascular component of coronary resistance.     

Lack of correlation between left ventricular mass and diameter of left coronary artery main trunk in hypertensive patients

The study was designed to evaluate whether the increase in left ventricular (LV) mass in essential hypertensives (H) is associated with a proportional increase in diameter of the left coronary artery (LCA) trunk. Twenty-six hypertensives, 14 with left ventricular hypertrophy (LVH) (left ventricular mass index [LVMI] ≥>134 g/m² in men and ≥110 g/m² in women) and 12 without LVH, and 10 normotensive controls (C) underwent clinical laboratory and echocardiographic transthoracic examination. LV dimensions were measured according to the Penn convention and LV mass calculated by the formula of Devereux. The LCA main trunk was visualized by two-dimension short axis view at the level of the great vessels section, and the diameter measured as intima–intima distance at end-diastole. Hypertensives with and without LVH and C had similar age, sex, and body surface area distribution. LVMI was, by definition, significantly higher in H with LVH than in H without LVH and in C (144 ± 21, 113 ± 13, and 98 ± 10 g/m², P < .01), whereas the diameter of the LCA trunk was similar in all groups (0.48 ± 0.1, 0.48, and 0.46 cm, respectively). There was no significant correlation between LVMI and LCA diameter in H (r = 0.21, P = not significant). The diameter of LCA trunk was significantly correlated only with BSA (r = 0.5, P < .01), LV end-systolic and end-diastolic diameters (r = 0.5 and r = 0.4, P < .05). Our data suggest that in H the increase in LVM is not associated with a concomitant increase of epicardial coronary artery diameter, and this finding may account in part for the impairment of coronary blood flow reserve in LVH.     

Cardiac function in sickle cell anemia

Although ventricular dysfunction is suspected to underlie congestive heart failure in sickle cell anemia (SCA), ejection indexes of left ventricular (LV) pump performance have been found to be normal. The increased preload and decreased afterload of SCA increases the ejection phase indexes and might obscure true LV dysfunction. Therefore, the preload and afterload independent end-systolic stress-volume index was compared in 11 patients with SCA and in 11 normal volunteers. End-systolic pressure and echocardiographic LV dimensions were determined during rest, leg raise, hand-grip and amyl nitrite inhalation. Systemic vascular resistance (afterload) was decreased to 1,033 ± 314 dynes s cm⁻⁵ (mean ± standard deviation) in SCA from 1,701 ± 314 dynes s cm⁻⁵ in normal subjects. End-diastolic volume index (preload) was increased to 102 ± 24 ml/m² in SCA from 66 ± 10 ml/m² in normal subjects. Cardiac index was increased to 4.7 ± 1.1 liters/min/m² in SCA from 2.8 ± 0.8 liters/ min/m² in normal subjects. Ejection fractions were similar: 0.59 ± 0.09 in SCA versus 0.62 ± 0.07 in normal subjects. However, in patients with SCA, the ratio of resting end-systolic stress-volume index was decreased (1.5 ± 0.5 in SCA versus 2.8 ± 0.6 in normal subjects) and the slope of the end-systolic stress versus end-systolic volume index relation was decreased (2.7 ± 1.3 in SCA versus 4.4 ± 1.8 in normal subjects), suggesting LV dysfunction in those patients. Thus, LV muscle contractile performance is depressed in SCA. Increased preload and decreased afterload compensate for the LV dysfunction and maintain a normal ejection fraction and high cardiac output.     

Diagnosis of increased pulmonary blood flow by suprasternal M-mode echocardiography in atrial septal defect

The right pulmonary artery (PA) was quantitatively assessed by Suprasternal M-mode echocardiography in 25 patients in whom an atrial septal defect (ASD) was suspected clinically. In 10 patients an ASD was excluded (Group 1) and in 15 it was confirmed (Group 2). The smallest diameter of the right PA at end-diastole in Group 1 was 8.8 ± 1.5 mm/m² body surface area and in Group 2 14.8 ± 3.6 mm/m² (p < 0.001). The greatest diameter of the right PA during systole was also much smaller in Group 1 (11.3 ± 1.2 mm/m²) than in Group 2 (17.7 ± 3.5 mm/m²) (p < 0.001). The absolute and percent systolic expansion of the right PA did not differ in the 2 groups (2.7 ± 0.5 mm [29.1 ± 10.8%] in Group 1 and 2.9 ± 0.8 mm [20.8 ± 9.8%] in Group 2). No correlation was found between measured and derived echocardiographic variables of the right PA and the magnitude of the left-to-right shunt. Patients in Group 2, who had an additional pressure elevation in the PA, showed, on average, a larger right PA and a smaller percent systolic expansion. The study demonstrates characteristic alterations in the wall motion pattern of the right PA in patients with ASD, indicating increased pulmonary blood flow.