Spherical Ventricle Research Articles

Predictors of functional mitral regurgitation recurrence after percutaneous mitral valve repair

We aimed to identify predictors of mitral regurgitation recurrence (MR) after percutaneous mitral valve repair (PMVR) in patients with functional mitral regurgitation (FMR). Patients with FMR were enrolled who underwent PMVR using the MitraClip® device. Procedural success was defined as reduction of MR of at least one grade to MR grade ≤ 2 + assessed at discharge. Recurrence of MR was defined as MR grade 3 + or worse at one year after initially successful PMVR. A total of 306 patients with FMR underwent PMVR procedure. In 279 out of 306 patients (91.2%), PMVR was successfully performed with MR grade ≤ 2 + at discharge. In 11.4% of these patients, MR recurrence of initial successful PMVR after 1 year was observed. Recurrence of MR was associated with a higher rate of heart failure rehospitalization during the 12 months follow-up (52.0% vs. 30.3%; p = 0.029), and less improvement in New York Heart Association (NYHA) functional class [68% vs. 19% of the patients presenting with NYHA functional class III or IV one year after PMVR when compared to patients without recurrence (p = 0.001)]. Patients with MR recurrence were characterized by a higher left ventricular sphericity index {0.69 [Interquartile range (IQR) 0.64, 0.74] vs. 0.65 (IQR 0.58, 0.70), p = 0.003}, a larger left atrium volume [118 (IQR 96, 143) ml vs. 102 (IQR 84, 123) ml, p = 0.019], a larger tenting height 10 (IQR 9, 13) mm vs. 8 (IQR 7, 11) mm (p = 0.047), and a larger mitral valve annulus [41 (IQR 38, 43) mm vs. 39 (IQR 36, 40) mm, p = 0.015] when compared to patients with durable optimal long-term results. In a multivariate regression model, the left ventricular sphericity index [Odds Ratio (OR) 1.120, 95% Confidence Interval (CI) 1.039–1.413, p = 0.003)], tenting height (OR 1.207, 95% CI 1.031–1.413, p = 0.019), and left atrium enlargement (OR 1.018, 95% CI 1.000–1.038, p = 0.047) were predictors for MR recurrence after 1 year. In patients with FMR, baseline parameters of advanced heart failure such as spherical ventricle, tenting height and a large left atrium might indicate risk of recurrent MR one year after PMVR.

Ventricular reshaping with a beating heart implant improves pump function in experimental heart failure

ObjectiveThe left ventricle remodels from an ellipsoidal/conical shape to a spherical shape after a myocardial infarction. The spherical ventricle is inefficient as a pumping chamber, has higher wall stresses, and can lead to congestive heart failure. We sought to investigate if restoring physiological ventricular shape with a beating heart implant improves pump function. MethodsRats were induced with a myocardial infarction, developing left ventricular dilatation and dysfunction, and becoming spherical over 3 weeks. Thereafter, they were randomized to undergo left ventricular reshaping with a beating heart implant (n = 19) or continue follow-up without an implant (n = 19). Biweekly echocardiography was performed until 12 weeks, with half the rats euthanized at 6 weeks and remaining at 12 weeks. At termination, invasive hemodynamic parameters and histopathology were performed. ResultsAt 3 weeks after the infarction, rats had a 22% fall in ejection fraction, 31% rise in end diastolic volume, and 23% rise in sphericity. Transventricular implant reshaping reduced the volume by 12.6% and sphericity by 21%, restoring physiologic ventricular shape and wall stress. Over the 12-week follow-up, pump function improved significantly with better ventricular-vascular coupling in the reshaped hearts. In this group, cardiomyocyte cross-section area was higher and the cells were less elongated. ConclusionsReshaping a postinfarction, failing left ventricle to restore its physiological conical shape significantly improves long-term pump function.

A case report of myocarditis combined with hepatitis caused by herpes simplex virus

BackgroundViral myocarditis presents with various symptoms, including fatal arrhythmia and cardiogenic shock, and may develop into chronic myocarditis and dilated cardiomyopathy in some patients. We report a case of viral myocarditis and hepatitis caused by herpes simplex virus.Case presentationA 20-year-old woman was admitted to our hospital with fever, fatigue, and anorexia. The initial investigation showed elevated liver enzyme levels and elevated creatine phosphokinase, and computed tomography showed diffuse swelling and internal heterogeneous image in the liver. These findings were consistent with acute hepatitis; therefore, we performed a liver biopsy, which showed parenchymal necrosis and lymphocytic infiltration. The night that the liver biopsy was performed, blood pressure gradually decreased and revealed cardiogenic shock. Electrocardiography showed diffuse ST-segment elevation, and echocardiography showed a dilated, spherical ventricle with reduced systolic function and pericardial effusion. An endomyocardial biopsy revealed lymphocyte infiltration of the myocardium, confirming acute myocarditis. After a few days, tests for immunoglobin M and immunoglobin G antibodies against herpes simplex virus were positive.ConclusionsWe presented a rare case of myocarditis combined with hepatitis that was caused by herpes simplex virus. Acute myocarditis can occur concurrently with hepatitis, pancreatitis, nephritis, and encephalitis; thus, determining the presence of other infectious lesions is necessary to provide appropriate treatment for the patient.

Usefulness of Left Atrial Reservoir Size and Left Ventricular Untwisting Rate for Predicting Outcome in Primary Mitral Regurgitation

The present study proposed to evaluate whether analysis of cardiac mechanics through speckle-tracking imaging is useful for risk stratification in asymptomatic patients with chronic primary mitral regurgitation (MR). We prospectively enrolled 67 patients (mean age 57 ± 18years) and followed them over time. MR was mild in 20 patients (30%), moderate in 24 (36%), and severe in 23 (34%). After a mean time of 24.8 ± 17months, 34 patients (51%) remained asymptomatic, whereas 33 (49%) developed events (19 underwent mitral valve surgery, 9 required hospitalization for acute heart failure, and 5 patients died). Compared to asymptomatic patients, those with events at baseline showed more severe MR, larger and spherical ventricles, diastolic dysfunction, and greater systolic pulmonary arterial pressure. Moreover, patients with events had decreased left atrial (LA) reservoir (p<0.001) and left ventricular (LV) untwisting rate (p <0.001). On univariate Cox regression analysis, effective regurgitant orifice area (p <0.001), vena contracta (p <0.001), systolic pulmonary arterial pressure (p= 0.003), LV end-systolic diameter (p <0.001), E/E' ratio (p= 0.004), LA volume (p= 0.001), LA reservoir (p <0.001), and LV untwisting rate (p <0.001) were associated with an increased risk of events. On multivariate analysis, only LA reservoir (p= 0.013) and LV untwisting rate were independent predictors (p= 0.017) of outcome. Moreover, LA reservoir evaluation significantly improved (p= 0.013) risk stratification compared to recommended parameters. In conclusion, impaired cardiac mechanics is more closely associated than severity of MR with the occurrence of events in asymptomatic chronic primary MR.

Outcomes of left ventricular reconstruction when established parameters are followed, and subsequent questions

The 2010 Task Force guidelines from the European Society of Cardiology/European Association of Cardiothoracic Surgery (ESC/EACTS) recommend ‘consideration of surgical ventricular restoration (SVR) to treat ischemic dilated cardiomyopathy, following measurement of ventricular volume and assessment of myocardial scar in centers with high experience’ [1]. This issue contains a report by Cho et al. [2] concerning ‘Long-term results and mid-term features of left ventricular reconstruction procedures on left ventricular volume, geometry, function and mitral regurgitation’ that amplifies the importance of surgical ventricular restoration (SVR) to architecturally remedy the failing hearts of patients with ischaemic dilated cardiomyopathy. Their superb results confirm how this procedure carries a very low perioperative mortality (1.6%), dramatically diminishes rehospitalization for cardiac causes over a 7-year interval and allows 79% long-term survival. These beneficial results are in concert with the broad number of world-wide SVR reports [3] and thus provide yet another contradiction to the flawed Surgical Treatment for Ischemic Heart Failure (STICH) study [4], whose misguided results have caused global curtailment of properly treating ischaemic dilated cardiomyopathy. Cho et al. precisely followed the benchmark SVR entry criteria of >60 ml/m left ventricular end-systolic volume index (LVESVI), >35% scarring of the left ventricle (LV) perimeter and achieved the requisite 40% reduction of ventricular volume to reduce the LVESVI of <60 ml/m. These SVR-induced changes show why LVESVI <60 ml/m is an independent predictor of prognosis [5], as the very low 7-year mortality ‘resulted from the natural events of neoplasm and infection’ rather than from pump failure or sudden death. These splendid results were similarly achieved by the Dor, linear closure and septal anterior ventricular exclusion (SAVE) procedures, yet each outcome was accompanied by creating a more spherical ventricle instead of the intended elliptical form. Confirmation of improved systolic performance was garnered from the increased systolic eccentricity index that indicated the smaller remote muscle contracted more efficiently as it became more helical during ejection. Moreover, late findings in patients with larger pre-SVR ventricular volumes showed the development of a 22% incidence of mitral regurgitation (MR), which parallels Di Donato’s report of 38% later mitral insufficiency in patients with even larger preoperative ventricular volumes [6]. These shape and MR change direct attention towards how the procedure execution influenced these findings, since Pocar recently pointed out the disadvantage of a more spherical chamber and functional MR [7].

Induction of Manganese Superoxide Dismutase by Nuclear Translocation and Activation of SIRT1 Promotes Cell Survival in Chronic Heart Failure

Oxidative stress plays a pivotal role in chronic heart failure. SIRT1, an NAD(+)-dependent histone/protein deacetylase, promotes cell survival under oxidative stress when it is expressed in the nucleus. However, adult cardiomyocytes predominantly express SIRT1 in the cytoplasm, and its function has not been elucidated. The purpose of this study was to investigate the functional role of SIRT1 in the heart and the potential use of SIRT1 in therapy for heart failure. We investigated the subcellular localization of SIRT1 in cardiomyocytes and its impact on cell survival. SIRT1 accumulated in the nucleus of cardiomyocytes in the failing hearts of TO-2 hamsters, postmyocardial infarction rats, and a dilated cardiomyopathy patient but not in control healthy hearts. Nuclear but not cytoplasmic SIRT1-induced manganese superoxide dismutase (Mn-SOD), which was further enhanced by resveratrol, and increased the resistance of C2C12 myoblasts to oxidative stress. Resveratrol's enhancement of Mn-SOD levels depended on the level of nuclear SIRT1, and it suppressed the cell death induced by antimycin A or angiotensin II. The cell-protective effects of nuclear SIRT1 or resveratrol were canceled by the Mn-SOD small interfering RNA or SIRT1 small interfering RNA. The oral administration of resveratrol to TO-2 hamsters increased Mn-SOD levels in cardiomyocytes, suppressed fibrosis, preserved cardiac function, and significantly improved survival. Thus, Mn-SOD induced by resveratrol via nuclear SIRT1 reduced oxidative stress and participated in cardiomyocyte protection. SIRT1 activators such as resveratrol could be novel therapeutic tools for the treatment of chronic heart failure.

Surgical Treatment of Left Ventricular Aneurysms: A Comparison of Long-term Follow-up of Left Ventricular Function for Classic Aneurysmectomy and Endoaneurysmorrhaphy Techniques

Myocardial infarction may be complicated by the formation of a left ventricular (LV) aneurysm that distorts the normal elliptical geometry of the ventricle to produce a dilated spherical ventricle with limited contractile and filling capacities. One of the consequences is congestive heart failure, which may be refractory to medical therapy and require surgical treatment. The aim of this study was to evaluate LV function in the late term following repair of LV aneurysm. Ninety-seven patients underwent repair of postinfarctional LV aneurysms. Sixty-one patients (62.9%) underwent classic aneurysmectomy, and 36 patients (37.1%) had endoaneurysmorrhaphy. The mean age (+/-SD) of the 87 men (89.7%) and 10 women was 55.98 +/- 8.59 years. Coronary surgery was performed in 82 patients (84.5%), with a mean of 1.34 +/- 0.77 grafts/patient. The mean preoperative ejection fraction (EF) was 39.74% +/- 8.79% (classic, 39.92% +/- 8.90%; endoaneurysmorrhaphy, 39.43% +/- 8.61%; difference not statistically significant [NS]). Fifty-five patients (56.7%) had angina of Canadian Cardiovascular Society class III to IV (classic, 55.7%; endoaneurysmorrhaphy, 58.3%; NS), 31 patients (31.9%) were in New York Heart Association (NYHA) class III to IV (classic, 31.1%; endoaneurysmorrhaphy, 33.3%; NS), and the mean preoperative NYHA functional class was 2.88 +/- 0.74 (classic, 2.83 +/- 0.77; endoaneurysmorrhaphy, 2.97 +/- 0.71; NS). The mortality rate at <30 days was 9.8% (n = 6) in the classic aneurysmectomy group and 2.7% (n = 1) in the endoaneurysmorrhaphy group. Long-term follow-up was available for 80 of these patients. During a mean follow-up of 79.3 +/- 37.6 months (range, 6-156 months), 14 patients (17.5%) died of a cardiac-related cause (classic, 8 patients [16.6%]; endoaneurysmorrhaphy, 6 patients [18.7%]; NS). The cardiac-related survival rate was 82.5%. In the first year, at 5 years, and at 10 years, the survival rates of the patients who underwent classical aneurysmectomy were 98.8%, 93.5%, and 76.1%, respectively, and the rates for patients who underwent endoaneurysmorrhaphy were 100%, 93.0%, 71.2%, respectively (P = .2). In the follow-up patient population, the mean preoperative EF was 40.21% +/- 9.44% in the classic aneurysmectomy group and 39.34% +/- 8.61% in the endoaneurysmorrhaphy group. Postoperatively, mean EFs increased to 44.24% +/- 9.50% and 43.80% +/- 8.81%, respectively, at the last follow-up. NYHA functional class changed from 2.79 +/- 0.77 preoperatively to 1.60 +/- 0.73 postoperatively in the classic aneurysmectomy group and from 2.97 +/- 0.71 preoperatively to 1.34 +/- 0.54 postoperatively in the endoaneurysmorrhaphy group. There was no significant difference in hospital readmissions for cardiac causes (classic, 27.1%; endoaneurysmorrhaphy, 31.2%). LV aneurysm can be repaired with acceptable surgical risk. Surgical treatment of LV aneurysm is associated with an improvement in long-term survival and symptoms.

Left-ventricular aneurysms: from disease to repair

Myocardial infarction may be complicated by the formation of a left-ventricular aneurysm that distorts the normal elliptical geometry of the ventricle to produce a dilated spherical ventricle with limited contractile and filling capacities. One of the consequences is congestive heart failure, which may be refractory to medical therapy and require surgical treatment. Surgical methods to restore the volume and shape of the left ventricle have evolved over the years. Nevertheless, although surgery for left-ventricular aneurysms has been performed for almost 50 years, the most appropriate approach is still controversial. This review gives an overview of the postinfarction left-ventricular aneurysm, tackling issues from the disease itself to surgical and other techniques of ventricular remodeling.

Why the left ventricle is not a sphere

Abstract In this study, we have tried to understand why the left ventricle (LV) is not a homogeneous sphere. An experimental model of a spherical ventricle was developed. The chamber was configured as a mathematical model, and the wall properties were represented by isolated cardiac muscles. The stroke work of the spherical LV when modelling different types of inhomogeneity in the wall structure was investigated. It was found that the emergence of even slight inhomogeneity in a spherical ventricle inevitably results in a diminution of pump function. It was concluded that at a given level of the myocardial contractility, a homogeneous spherical LV would not have any functional reserve, ie no ability to maintain pump function in case of additional load. Functional reserve can be achieved only with a certain degree of inhomogeneity. Thus, inhomogeneity in the normal left ventricular wall structure constitutes a strategic functional reserve that is absent in a homogeneous spherical ventricle.

Why the left ventricle is not a sphere

In this study, we have tried to understand why the left ventricle LV is not a homogeneous sphere. An experimental model of a spherical ventricle was developed. The chamber was configured as a mathematical model, and the wall properties were represented by isolated cardiac muscles. The stroke work of the spherical LV when modelling different types of inhomogeneity in the wall structure was investigated. It was found that the emergence of even slight inhomogeneity in a spherical ventricle inevitably results in a diminution of pump function. It was concluded that at a given level of the myocardial contractility, a homogeneous spherical LV would not have any functional reserve, ie no ability to maintain pump function in case of additional load. Functional reserve can be achieved only with a certain degree of inhomogeneity. Thus, inhomogeneity in the normal left ventricular wall structure constitutes a strategic functional reserve that is absent in a homogeneous spherical ventricle.

Why the Left Ventricle Is Not a Sphere

In this study, we have tried to understand why the left ventricle (LV) is not a homogeneous sphere. An experimental model of a spherical ventricle was developed. The chamber was configured as a mathematical model, and the wall properties were represented by isolated cardiac muscles. The stroke work of the spherical LV when modelling different types of inhomogeneity in the wall structure was investigated. It was found that the emergence of even slight inhomogeneity in a spherical ventricle inevitably results in a diminution of pump function. It was concluded that at a given level of the myocardial contractility, a homogeneous spherical LV would not have any functional reserve, ie no ability to maintain pump function in case of additional load. Functional reserve can be achieved only with a certain degree of inhomogeneity. Thus, inhomogeneity in the normal left ventricular wall structure constitutes a strategic functional reserve that is absent in a homogeneous spherical ventricle.

Echocardiographic analysis of regional and global left ventricular shape in chagas’ cardiomyopathy

Chagas’ heart disease is a common form of cardiomyopathy in Latin America and an important cause of cardiac morbidity and mortality there. Left ventricular (LV) apical aneurysm and LV dysfunction are frequent findings in Chagas’ cardiomyopathy. Because cardiac shape has important implications for LV function, we sought to characterize regional and global changes in LV geometry in Chagas’ heart disease. Quantitative shape analysis was performed on 2-dimensional echocardiograms from 43 patients with Chagas’ cardiomyopathy. Regional shape was quantitated by measuring endocardial curvature and global shape was evaluated by Fourier shape analysis of the endocardial contour. Data from 22 age- and sex-matched normal test subjects were used for comparison. Regional shape analysis demonstrated decreased apical curvature (consistent with blunting of normal apical shape) in the group with Chagas’ disease compared with controls (apical 2-chamber view: 19 ± 1 vs 24 ± 1 [p = 0.0039] at end-diastole and 20 ± 2 vs 29 ± 3 [p = 0.0019] at end-systole). Fourier shape power index was decreased in the Chagas’ group, consistent with a more spherical ventricle (apical 2-chamber view: 9 ± 1 vs 17 ± 2 [p <0.0001] at end-diastole and 12 ± 1 vs 35 ± 3 [p <0.0001] at end-systole). Shape changes among the population with Chagas’ disease were further evaluated in those with end-diastolic volumes equal to or greater than the median for the group (104 ml) and those <104 ml. Global shape did not differ between patients with dilated ventricles and those with relatively nondilated ventricles. Diastolic Fourier shape power index = 8 ± 2 in dilated ventricles compared with 9 ± 5 in nondilated ventricles (p = 0.53); systolic Fourier shape power index = 10 ± 2 in dilated versus 14 ± 2 in nondilated ventricles (p = 0.15) (apical 2-chamber view). In Chagas’ cardiomyopathy, LV apical deformation results in disruption of the optimal global prolate-ellipsoid shape, even in patients with relatively preserved LV volumes.

Relation of ventricular size and function to heart failure status and ventricular dysrhythmia in patients with severe left ventricular dysfunction

Patients with severe left ventricular (LV) dysfunction may or may not have overt heart failure and ventricular dysrhythmia. To study factors behind this variability, we examined a subset of 311 patients from the Studies of Left Ventricular Dysfunction—95 with a history of moderate heart failure (treatment trial) and 216 with no failure (prevention trial), all with ejection fractions <0.35. Echocardiographic variables were compared between trials and also correlated with dysrhythmia in 258 patients, and with neurohormones in 199 patients. Compared with prevention patients, treatment patients had larger LV end-diastolic diameter, end-systolic volume, sphericity index, and ratio of early to late diastolic filling velocity by Doppler ( E A ratio), lower LV ejection fraction and atrial contribution to ventricular filling, and similar LV mass, end-diastolic volume, and estimates of systolic wall stress. With prevention and treatment patients combined, the prevalence of abnormally elevated atrial natriuretic peptide was 92% in the highest fertile of E A ratio compared with 55% in the lower fertiles (p = 0.006). Across fertiles of LV end-diastolic volume, there was an increase in the prevalence of nonsustained ventricular tachycardia (24%, 45%, and 45%; p = 0.007) and premature ventricular complexes > 10/hour (48%, 62%, and 80%; p < 0.001). Thus, in severe LV dysfunction, ventricular filling indexes suggestive of high filling pressures, along with larger and more spherical ventricles, are particularly common in patients with overt heart failure, thus suggesting that diastolic properties and the degree of ventricular remodeling affect clinical status. Once ejection fraction is significantly reduced, the prevalence of ventricular dysrhythmia correlates with LV size rather than systolic function. This observation lends support to previous experimental findings on the role of myocardial stretch and scar in the genesis of dysrhythmia.

A simulation of three-dimensional systolic flow dynamics in a spherical ventricle: effects of abnormal wall motion.

Alterations in left ventricle (LV) wall motion induced by ischemia will affect flow dynamics, and these altered flow fields can be used to evaluate LV pumping efficiency. LV chamber flow fields were obtained in this study by solving the discretized three-dimensional Navier-Stokes equations for viscous, incompressible unsteady flow by using the finite analytic method. Several cases of abnormal wall motion (AWM) were simulated by a manipulation of the boundary conditions to produce regions of hypokinesis, akinesis, and dyskinesis. These solutions were used to determine the central ejection region (CER), defined as the region of flow domain in which the obtained velocity field vectors are aligned +/- 3 degrees from the LV long axis. A CER coefficient was computed from information on the location and orientation of the CER within the LV cavity. Contraction of the spherical ventricle produced a vector field that was symmetric with respect to the long axis. For the simulations of AWM, an asymmetrical flow pattern developed, became more pronounced with increasing severity of AWM, and resulted in a shorter CER that shifted toward the ischemic region. The CER coefficients decreased monotonically with increased severity in AWM from 0.948 in the normal case to a low of 0.164 for the most severe case of AWM. The CER coefficient quantitatively displayed the sensitivity of the flow patterns to even moderate degrees of hypokinesis. In addition, visualization of the three-dimensional flow field reinforced the necessity of three-dimensional simulations to capture aspects of the flow that existing methods of two-dimensional flow imaging that use ultrasound may miss.

Repair of left ventricular aneurysm

Anteroapical left ventricular aneurysms were produced in 23 sheep by coronary arterial ligation. Plication of the aneurysm does not change stroke volume or cardiac output and does not significantly change left ventricular oxygen consumption from the preoperative value of 5.1 +/- 2.6 ml/100 gm per minute. Plication, however, does increase left ventricular end-systolic elastance from 3.2 +/- 0.9 to 4.4 +/- 1.5 mm Hg/mm (p = 0.005). In nine of these sheep the midsagittal plane of the left ventricle was imaged by means of an array of sonomicrometry crystals before and after plication of the aneurysm. Regional wall stresses at end-systole and end-diastole and changes in diastolic function were calculated for anterior and posterior ventricular walls in the border zone adjacent to the aneurysm and in more basilar myocardium remote from the infarct. Plication significantly reduced end-systolic wall stresses and systolic stress integrals in the posterior border zone and remote myocardium, but it did not significantly change anterior wall systolic stresses or stress integrals. Plication also decreased diastolic stretching of border zone myocardium. Plication of anteroapical left ventricular aneurysm produced a shorter, more spherical ventricle and removed the dyskinetic segments but altered deformation (strain) in both circumferential and longitudinal directions. The changes in ventricular wall geometry and deformation provide an explanation for the increased ventricular end-systolic elastance and unchanged stroke volume observed after aneurysm plication.

Effects of left ventricular shape and captopril therapy on exercise capacity after anterior wall acute myocardial infarction

The importance of left ventricular (LV) shape in determining exercise capacity was assessed in 40 male patients with LV dysfunction after anterior acute myocardial infarction (AMI). Because captopril therapy is known to improve exercise capacity in this patient population, the potential interaction between LV shape and captopril therapy was also evaluated. Patients underwent cardiac catheterization 2 to 4 weeks after AMI followed by randomization to receive placebo or captopril. LV shape was defined from biplane ventriculography by a sphericity index (volume observed/volume of sphere using long axis as diameter). Quarterly clinical assessments and maximal exercise testing were performed. A cumulative heart failure score, specific activity scale and average exercise time for the year were calculated. A greater shape distortion (increasing sphericity index) was associated with increased LV volumes, decreased ejection fraction and a larger abnormally contracting segment. Sphericity index was the only independent predictor of average exercise duration in the placebo group. Placebo-treated patients in the tercile with the most spherical ventricles had not only the lowest exercise capacity (p < 0.01), but also accumulated the highest heart failure (p < 0.05) and specific activity scale (p < 0.05) scores. Captopril-treated patients with the same baseline distortion of LV shape did not manifest these shape-dependent objective and subjective measures of reduced functional capacity.

Left ventricular shape, afterload and survival in idiopathic dilated cardiomyopathy

Because idiopathic dilated cardiomyopathy is characterized by elevated wall stress and a more spherical left ventricle, the relations among shape, afterload and survival were examined. Thirty-six patients with cardiomyopathy were prospectively studied by two-dimensional echocardiography. Data included echocardiographic short- and long-axis cavity dimensions, their ratio and, with cuff systolic blood pressure, meridional and circumferential end-systolic stresses and their ratios. Survivors (n = 16) were followed up for 52 months (range 40 to 76); nonsurvivors (n = 20) died an average of 11 months after study.Survivors had a smaller left ventricular end-diastolic short-axis dimension (6.4 versus 7.1 cm, p < 0.03) but a similar long-axis length (8.6 versus 8.3 cm). However, overall cavity shape or the ratio of short- to long-axis end-diastolic dimensions was more spherical in those with poorer survival (ratio 0.76 versus 0.68, p 0.02). Meridional and circumferential end-systolic stresses were similar in the two groups, but stress was more evenly distributed in the long- and short-axis planes in nonsurvivors (meridional/circumferential stress ratio 0.57 versus 0.52 in survivors, p < 0.05). Improved survival was associated with an end-diastolic short-axis dimension <7.6 cm, a short- to long-axis ratio <0.76 and a meridional to circumferential stress ratio <0.54. Life table analysis revealed a 28% mortality rate in patients with all three of these characteristics compared with 100% in patients with none. Survivors and nonsurvivors did not differ in systolic cavity dimension, wall thickness, relative wall thickness, cavity volume, percent posterior wall thickening or fractional shortening.In conclusion, a poorer survival was associated with a more spherical ventricle and a more uniform distribution of afterload. In contrast, there was no association between survival and wall thickness, systolic function and endsystolic stress. Two-dimensional echocardiographic determinations of cavity dimension, shape and load distribution may provide useful prognostic information in dilated cardiomyopathy.

Pressure-velocity relation in the isolated rabbit left ventricle.

The relation between pressure (P) and ejection velocity (V) was determined in the coronary-perfused rabbit left ventricle. The heart was isolated and a thin latex balloon was inserted into the left ventricle. The volume of the ventricle was changed at a constant velocity with a magnetic shaker connected to the balloon at various phases of contraction and the corresponding pressure change was measured. The pressure-velocity relation determined by this isovelocity method was well fitted by a hyperbolic equation, (P + A) (V + B) = B(PO + A), where A and B are constants and Po is the maximum systolic pressure. Using the thick-walled spherical ventricle model, the Hill equation of the ventricular wall muscle with constants a and b was obtained, and Hill constants (a and b) were calculated from ventricular constants (A and B). The constants A and B/V (V is the volume of ventricle) increased with decreases in ventricular volume, but the ratio Vmax/TO (= b/aL, L is the length of the muscle) was not affected. The value of Vmax/TO was 1.14 +/- 0.22 X 10(-5) cm2/(dyn X sec) (mean +/- S. D. in 9 rabbits). The constants A and B/V, especially A, increased and the ratio Vmax/TO decreased under the negative inotropic effect, such as decreased heart rate or decreased coronary perfusion pressure. This ratio would therefore be a good indicator for assessment of the ventricular performance as well as the contractility of the wall muscle.

An index of the contractile state of the myocardium in man.

There is a profound need, on both clinical and physiologic grounds, for a measure of the contractile state of the intact ventricle. Such a measure can be obtained by evaluating the force-velocity relationship with a correction for myocardial fiber length. The force-velocity relation can be expressed as the ratio of maximum rate of pressure rise to maximum isovolumetric pressure, a quantity which was described by Hill as the maximum rate of proportional rise of pressure and which is similar to the velocity constant of a chemical reaction. Division of this ratio by an estimate of ventricular circumference corrects for variations due to differences in initial fiber length. This index was evaluated in 11 normal subjects and 46 patients with cardiac disease during left heart catheterization. Maximum rate of pressure rise was obtained by electronic differentiation of the ventricular pressure pulse, and ventricular circumference, assuming a spherical ventricle, was calculated from volumes measured by indicator washout. The contractility index of normal subjects did not differ from that of patients with mitral stenosis, atrial septal defect, or chronic pulmonary disease (patients without left ventricular overloading). In contrast, in patients with left ventricular failure, the indices were more than two standard deviations below the mean value for normal subjects. Such a reduction was not noted in patients with pressure or volume overloading of the left ventricle before the onset of myocardial failure. During exercise, the index rose uniformly in patients without left ventricular disease, responded variably in compensated patients with volume or pressure overloading, and was virtually unchanged in patients with left ventricular decompensation. The administration of isoproterenol or digitalis resulted in increased contractility regardless of the patient's status. It is concluded that the use of this index in physiologic studies of the ventricle and in diagnostic and therapeutic decisions is justified.