Large Left Ventricular Research Articles

Predictors of Mortality and Hospitalization for Cardiac Causes in Patients with Heart Failure and Nonischemic Heart Disease: A Subanalysis of the ALPHA Study

Several studies have searched for predictors of clinical outcome in patients with heart failure (HF). However, since they were collected in clinical trials, most data were subject to selection biases and do not specifically apply to patients with nonischemic heart disease. This study examined the impact of several variables on combined all-cause mortality and hospitalization for cardiac causes, in consecutive ambulatory patients with HF included in the ALPHA registry. This analysis included 446 patients with HF and nonischemic heart disease, in New York Heart Association functional class II or III, and a left ventricular (LV) ejection fraction below 40%. In 126 patients (73%) the disease was idiopathic dilated cardiomyopathy, in 72 (16%) hypertensive, in nine (2%) valvular, and in 39 (9%) of other etiologies. The median age was 61 years (range 51-69 years) and 349 (78%) patients were men. Over a median follow-up of 31 months (range 23-40), 82 patients (18%) died or were hospitalized for cardiac causes. In a proportional hazard (Cox) regression model, maximal oxygen consumption (HR 0.9, P = 0.001), LV end-diastolic diameter (HR 1.07, P < 0.001), resting systolic blood pressure (HR 0.97, P < 0.005), and hemoglobin (HR 0.86, P < 0.05) were independent predictors of the combined study endpoint. In an unselected population of patients with HF and nonischemic heart disease, a reduced exercise capacity, large LV end-diastolic diameter, low systolic blood pressure, and hemoglobin were correlated with long-term all-cause mortality or hospitalization for cardiac causes. These observations may help stratifying and tailoring the treatment of patients with HF and nonischemic heart disease.

Unusual Cause of Heart Failure in a 65‐Year‐Old Woman

Left ventricular (LV) free wall rupture is a potentially lethal mechanical complication after myocardial infarction (MI). Pericardial adhesions or slow extracardiac leak and pericardial inflammation may result in a contained cardiac rupture. LV pseudoaneurysm is a relatively uncommon clinical entity. It may occur after MI, but also as a complication of infective endocarditis, cardiac surgery, or trauma. Patients developing LV pseudoaneurysm after MI may present angina pectoris or signs of congestive heart failure (HF) but often are asymptomatic. Surgery is the treatment of choice for LV pseudoaneurysms diagnosed in the first months after MI. The management of chronic LV pseudoaneurysms is still subject of debate. This report highlights a 65-year-old patient newly hospitalized for acute decompensated HF who was diagnosed with a large chronic LV pseudoaneurysm and severe mitral regurgitation. The patient underwent successful resection of the pseudoaneurysm and patch repair of the ruptured ventricular wall.

When should we close ventricular septal defects?

With the advent of catheter-based cardiac intervention, we are now capable of doing things that used to require open heart surgery in a less invasive manner. This progress has also allowed a thought process of potentially closing smaller and smaller ventricular septal defects (VSD). Important questions emerge about the appropriate indications for closure of VSD. In this issue of The Journal, Kleinman et al address these issues by reporting on a study of the natural history of unoperated patients with a moderate to large VSD and with left ventricular (LV) dilation. They found that most patients with pressure-restrictive VSDs, with moderate to large severe LV dilation, without heart failure, failure to thrive, or pulmonary hypertension will spontaneously decrease LV dilation over time without intervention. In an accompanying editorial, Beekman puts these findings in clinical perspective. He emphasizes that just because we can close VSDs without surgery, does not mean we should close them. He indicates that studies like that of Kleinman et al help to provide the evidence base we can use to make rational decisions about when to intervene. In most asymptomatic children with pressure restricted VSDs, even when they are relatively large, trans-catheter intervention is not needed to result in a favorable outcome. Spontaneous Regression of Left Ventricular Dilation in Children with Restrictive Ventricular Septal DefectsThe Journal of PediatricsVol. 150Issue 6PreviewTo test the hypothesis that left ventricular (LV) dilation associated with pressure-restrictive ventricular septal defect (VSD) often remains stable or regresses spontaneously, calling into question the role of interventional management for such defects. Full-Text PDF Closing the Ventricular Septal Defect Because You Can: Evidence-Averse Care?The Journal of PediatricsVol. 150Issue 6Preview“What this patient needs is a doctor.”—Eugene A. Stead, Jr, MD Full-Text PDF

Left ventricular myxoma originating from the interventricular septum and obstructing the left ventricular outflow tract

In a 60-year-old woman with episodic exertional faintness, a large left ventricular (LV) myxoma attached by a pedicle to the apical interventricular septum and prolapsing through the LV outflow tract and the aortic valve causing a severe obstruction was found by echocardiography. Early surgical excision was successfully performed using the transaortic approach.

Electrocardiographic response to enzyme replacement therapy for Pompe disease

PurposeElectrocardiogram (ECG) abnormalities are universal in infantile Pompe disease or glycogen storage disease type II, a fatal genetic muscle disorder caused by deficiency of acid α-glucosidase (GAA). Hallmarks of this disease include a shortened PR interval, an increased QT dispersion (QTd), and large left ventricular (LV) voltages. We evaluated the effect of recombinant human GAA (rhGAA) enzyme replacement therapy (ERT) on these ECG parameters in patients with infantile-onset Pompe disease. MethodsA total of 134 ECGs were evaluated from 19 patients (5 females and 14 males) with a median age of 5.5 months at the time of enrollment in open-label clinical trials exploring the safety and efficacy of ERT at a single center from 1999 to 2004. rhGAA was purified from genetically engineered Chinese hamster ovary cells overproducing GAA and infused intravenously at doses ranging from 10 mg/kg per week to 20 to 40 mg/kg every 2 weeks in patients with infantile-onset Pompe disease. The PR interval, QTd (longest to shortest QT), and LV voltage (SV1+RV6) were blindly determined by two independent observers. ResultsThe median follow-up period was 6 months (range 2–30 months). The PR interval lengthened from 83 (42–110) ms to 107 (95–130) ms (P < .001), and the QTd decreased from 83 (40–125) ms to 53 (20–80) ms (P = .003). There were significant decreases in LV voltage (67 [17–83] mV vs. 48 [18–77] mV, P = .03), which correlated with decrease in LV mass on two-dimensional echocardiogram. There was no evident change in the QTc interval (429 [390–480] ms vs. 413 [370–450] ms, P = not significant). ConclusionrhGAA ERT for infantile Pompe disease results in an increase in PR interval and a decrease in both the QTd and the LV voltage. These results suggest that these ECG parameters may be useful markers of the severity of cardiac disease and the response to ERT treatment in patients with infantile Pompe disease.

Visualization of a large ventricular aneurysm in a young man by 16-slice multi-detector row spiral computed tomography before successful surgical treatment

Left ventricular (LV) aneurysm after myocardial infarction without any clinical symptoms is a rare complication of coronary artery disease. In most cases, especially in young people, this complication is diagnosed too late, after rupture into the pericardial cavity has occurred. Here we present the successful surgical repair of a large LV aneurysm in a 35-year-old man. We could visualize this aneurysm and the coronary arteries non-invasively by contrast-enhanced 16-slice multi-detector row spiral computed tomography (MDCT).

Myocardial osteopontin expression is associated with collagen fibrillogenesis in human dilated cardiomyopathy

Osteopontin (OPN), an extracellular matrix (ECM) protein, plays an important role in myocardial remodeling by promoting collagen synthesis and accumulation in experimental animal models. We hypothesized that OPN could be expressed in myocardial tissues and contribute to collagen accumulation and myocardial dysfunction in human dilated cardiomyopathy (DCM). Endomyocardial biopsy tissues were obtained from 51 patients with DCM and 15 controls by right ventricular endomyocardial biopsy. OPN, collagen types I (Col I) and III (Col III) mRNA levels were measured by real-time reverse transcriptase polymerase chain reaction (RT-PCR). The cellular source of OPN was analyzed using immunohistochemistry and in situ hybridization. Myocardial collagen volume fraction (CVF) was determined by digital planimetry. OPN, Col I and Col III mRNA levels were higher in DCM patients than in controls (P<0.01). OPN mRNA levels were positively correlated with Col I levels and CVF in DCM patients (OPN vs. Col I: r=0.60, P<0.01; OPN vs. CVF: r=0.52, P<0.001). Immunostaining of OPN was present in cardiomyocytes from DCM patients. In situ hybridization identified cardiomyocytes as the major source of OPN mRNA transcription in DCM patients. OPN and Col I mRNA levels were highly expressed in the DCM subgroup with large left ventricular (LV) end-systolic diameter (LVESD > or = 54.5 mm) or low LV ejection fraction (LVEF < 29.5%). There was a weak positive correlation between OPN mRNA levels and LV end-systolic diameter (r=0.39, P<0.01). Levels of OPN mRNA were also negatively correlated with LV ejection fraction (r=-0.43, P<0.01). These results suggest that OPN may play a pivotal role in the development of Col-I-induced cardiac fibrosis and dysfunction in human DCM.

Extensive left ventricular remodeling does not allow viable myocardium to improve in left ventricular ejection fraction after revascularization and is associated with worse long-term prognosis.

Extensive left ventricular (LV) remodeling may not allow functional recovery after revascularization, despite the presence of viable myocardium. Seventy-nine consecutive patients with ischemic cardiomyopathy (left ventricle ejection fraction [LVEF] 29+/-7%) underwent surgical revascularization. Before revascularization, viability was assessed by metabolic imaging with F18-fluorodeoxyglucose and SPECT. LV volumes and LVEF were assessed by resting echocardiography. LVEF was re-assessed by echocardiography 8 to 12 months after revascularization. Three-year clinical follow-up (events: cardiac death, infarction, and hospitalization for heart failure) was also obtained. Forty-nine patients had substantial viability; 5 died before re-assessment of LVEF. Of the remaining 44 patients, 24 improved > or =5% in LVEF after revascularization, whereas 20 did not improve in LVEF. LV end-systolic volume was the only parameter that was significantly different between the groups (109+/-46 mL for the improvers versus 141+/-31 mL for the nonimprovers; P<0.05). The change in LVEF after revascularization was linearly related to the baseline LV end-systolic volume, with a higher LV end-systolic volume associated with a low likelihood of improvement in LVEF after revascularization. During the 3-year follow-up, the highest event-rate (67%) was observed in patients without viable myocardium with a large LV size, whereas the lowest event rate (5%) was observed in patients with viable myocardium and a small LV size. Intermediate event rates were observed in patients with viable myocardium and a large LV size (38%), and in patients without viable myocardium and a small LV size (24%). Extensive LV remodeling prohibits improvement in LVEF after revascularization and affects long-term prognosis negatively, despite the presence of viability.

Morphological and functional changes in cardiac myocytes isolated from mice overexpressing TNF-alpha.

Transgenic (TG) TNF1.6 mice, which cardiac specifically overexpress tumor necrosis factor-alpha (TNF-alpha), exhibit heart failure (HF) and increased mortality, which is markedly higher in young (<20 wk) males (TG-M) than females (TG-F). HF in this model may be partly caused by remodeling of the extracellular matrix and/or structure/function alterations at the single myocyte level. We studied left ventricular (LV) structure and function using echocardiography and LV myocyte morphometry, contractile function, and intracellular Ca(2+) (Ca(i)(2+)) handling using cell edge detection and fura 2 fluorescence, respectively, in 12-wk-old TG-M and TG-F mice and their wild-type (WT) littermates. TG-F mice showed LV hypertrophy without dilatation and only a small reduction of basal fractional shortening (FS) and response to isoproterenol (Iso). TG-M mice showed a large LV dilatation, higher mRNA levels of beta-myosin heavy chain and atrial natriuretic factor versus TG-F mice, reduced FS relative to both WT and TG-F mice, and minimal response to Iso. TG-F and TG-M myocytes were similarly elongated (by approximately 20%). The amplitude of Ca(i)(2+) transients and contractions and the response to Iso were comparable in WT and TG-F myocytes, whereas the time to 50% decline (TD(50%)) of the Ca(i)(2+) transient, an index of the rate of sarcoplasmic reticulum Ca(2+) uptake, was prolonged in TG-F myocytes. In TG-M myocytes, the amplitudes of Ca(i)(2+) transients and contractions were reduced, TD(50%) of the Ca(i)(2+) transient was prolonged, and the inotropic effect of Iso on Ca(i)(2+) transients was reduced approximately twofold versus WT myocytes. Protein expression of sarco(endo)plasmic reticulum Ca(2+)-ATPase 2 and phospholamban was unaltered in TG versus WT hearts, suggesting functional origins of impaired Ca(2+) handling in the former. These results indicate that cardiac-specific overexpression of TNF-alpha induces myocyte hypertrophy and gender-dependent alterations in Ca(i)(2+) handling and contractile function, which may at least partly account for changes in LV geometry and in vivo cardiac function in this model.

Impact of glucose intolerance and insulin resistance on cardiac structure and function: sex-related differences in the Framingham Heart Study.

Although insulin resistance has been implicated in the pathogenesis of left ventricular (LV) hypertrophy, previous studies have yielded inconsistent results and are limited by referral bias. We examined the relations between echocardiographic LV measurements and glucose tolerance status in 2623 Framingham Study subjects (1514 women, mean age 53 years) free of myocardial infarction and heart failure. We also evaluated the relations of insulin resistance (homeostasis model, HOMA-IR) and LV and left atrial (LA) measures within the normal and abnormal glucose tolerance categories (the latter included impaired glucose tolerance, impaired fasting glucose, and newly diagnosed diabetes). LV mass (adjusted for age, height, heart rate, and systolic blood pressure) increased across categories of worsening glucose tolerance; the trend was more striking in women (P<0.001) compared with men (P=0.054). In subjects with normal (n=2022) and abnormal glucose tolerance (n=327), covariate-adjusted LV mass and LV wall thickness increased across HOMA-IR quartiles in women (P<0.001) but not men. In contrast, covariate-adjusted LA size increased with worsening glucose tolerance and across HOMA-IR quartiles in the normal and abnormal glucose tolerance groups in both sexes. Adjustment for body mass index considerably attenuated the relations of LV/LA measures and HOMA-IR, rendering them statistically nonsignificant in the normal glucose tolerance group. In our large community-based sample, LV mass and wall thickness increased with worsening glucose intolerance, an effect that was more striking in women compared with men. Insulin resistance was associated with increased LV mass in women alone, but this relation was largely accounted for by obesity.

Estimation of preload recruitable stroke work relationship by a single-beat technique in humans

The slope of the preload recruitable stroke work relationship (M(w)) is a highly linear, load-insensitive contractile index. To investigate whether M(w) can be determined from a single steady-state beat, 45 patients were studied during cardiac catheterization. Single-beat M(w) (SBM(w)) was calculated directly from the baseline stroke work and baseline left ventricular (LV) end-diastolic volume (EDV(B)), and the volume-axis intercept (V(w)) was estimated as k x EDV(B) + (k - 1) x LV(wall), where k is the ratio of the epicardial shell volumes corresponding to V(w) and EDV(B) and LV(wall) is the wall volume. The mean of individual k values was 0.72 +/- 0.04, which correlated with LV mass significantly (r = 0.60, P < 0.001). SBM(w) calculated from a constant k of 0.7 predicted M(w) well (r = 0.88, P < 0.0001), and the prediction improved slightly when k was estimated from individual LV mass (r = 0.93, P < 0.0001). Subgroup analyses revealed that the single-beat technique also worked in patients with small or large LV mass or volume or with regional wall motion abnormalities. The absolute change in SBM(w) after dobutamine infusion also correlated with that in M(w). In conclusion, M(w) can be estimated from a steady-state beat without alteration of preload.

Time course of right ventricular remodeling in rats with experimental myocardial infarction.

Right ventricular (RV) weight increases dependent on time after myocardial infarction (MI) and on MI size. The sequential changes in RV volume and hemodynamics and their relations to left ventricular (LV) remodeling after MI are unknown. We therefore examined the time course of RV remodeling in rats with LV MI. MI was produced by left coronary artery ligation. Four, eight, and sixteen weeks later, LV and RV hemodynamic measurements were performed and pressure-volume curves were obtained. For serial measurement of RV volumes and performance, cine-MRI was performed 2 and 8 wk after MI. The ratios of beta-myosin heavy chain (MHC) to alpha-MHC and skeletal to cardiac alpha-actin were determined for the RV and LV after large MI or sham operation. RV weight increased in rats with MI, as did RV volume. RV pressure-volume curves were shifted toward larger volumes 16 wk after large MI. RV systolic pressure increased gradually over time; however, the gain in RV weight was always in excess of RV systolic pressure. The ratios of skeletal to cardiac alpha-actin and beta-MHC to alpha-MHC were increased after MI in both ventricles in a similar fashion. Because RV wall stress was not increased after infarction, mechanical factors may not conclusively explain hypertrophy, which maintained balanced loading conditions for the RV even after large LV infarction.

Relationship between plasma level of cardiotrophin-1 and left ventricular mass index in patients with dilated cardiomyopathy

OBJECTIVESThe study evaluated the relationship between plasma cardiotrophin-1 (CT-1) concentration and left ventricular (LV) mass in dilated cardiomyopathy (DCM) patients with congestive heart failure (CHF).BACKGROUNDCardiotrophin-1 is a newly identified member of the interleukin-6 (IL-6) family of cytokines and one of the endogenous ligands for gp130 signaling pathways in the heart, and it has potent hypertrophic and survival effects on cardiac myocytes. However, the clinical significance of CT-1 is poorly understood.METHODSWe measured the plasma CT-1 level in 51 consecutive patients with DCM. Patients were classified into two groups: small LV mass index group and large LV mass index group, based on the median level of LV mass index.RESULTSThe plasma CT-1 level was increased in DCM patients with the severity of CHF and was significantly higher in the large LV mass group than in the small LV mass group, despite the absence of a difference in LV ejection fraction between the two groups. In addition, there was a significant positive correlation between the plasma CT-1 level and the LV mass index (r = 0.627, p < 0.0001). According to stepwise multivariate analyses among hemodynamic and neurohumoral factors, a high plasma CT-1 level showed an independent and significant positive relationship with a large LV mass index in patients with DCM.CONCLUSIONSThese results indicate that the plasma CT-1 level is increased in patients with DCM and is significantly correlated with the LV mass index, suggesting that CT-1 plays an important role in structural LV remodeling in patients with DCM.

Postinfarction left-ventricular aneurysm: regional stress, function, and remodeling after aneurysmectomy.

Left-ventricular (LV) aneurysm formation after myocardial infarction (MI) leads to LV remodeling with global and regional cardiac dysfunction. LV aneurysmectomy (LVA) can often improve LV function, but changes of regional wall stress and systolic function in the noninfarcted segment before and after the operation remain poorly understood. The purpose of this study was to assess the effects of LVA on regional stress and systolic function in the noninfarcted region and to examine this procedure's impact on the LV remodeling in patients with LV aneurysm after myocardial infarction (MI). Using quantitative left ventriculography and pressure measurements, 11 patients with an anterior LV aneurysm were studied before and 8 months after standard linear repair (LVA group), and 10 patients with an anterior transmural infarction who received coronary artery bypass grafting were also studied (CABG group) in an attempt to separate the effects of aneurysmectomy from the effects of bypass surgery. Regional end-systolic (ESS) and end-diastolic (EDS) stresses of the contractile segment (CS) were computed by Janz's method. The total ejection fraction (EF) increased (p < 0.01) in the LVA group, whereas it did not change in the CABG group at 8 months after surgery. Both the end-diastolic and end-systolic volume indices of CS decreased (p < 0.01 and p < 0.01, respectively) in the LVA group, whereas both remained unchanged in the CABG group. The mean velocity of circumferential fiber shortening (mean Vcf) of CS increased substantially (p < 0.01) in the LVA group and, less significantly (p < 0.05), in the CABG group. Regional ESS and EDS decreased (p < 0.01 and p < 0.05, respectively) in the LVA group, whereas both remained unchanged in the CABG group. The increase in mean Vcf correlated strongly with the magnitude of decrease in ESS (r = -0.63, p < 0.01) in the LVA group but not in the CABG group. LVA can reduce regional afterload and improve ejection performance of the noninfarcted myocardium in many patients with a large anterior LV aneurysm and, moreover, may favorably affect the LV remodeling process after MI.

The relationship between R amplitude in lead V5 (RV5) and left ventricular mass in the groups of adolescent subjects classified by body composition.

How the amplitude of the R wave in lead V5 (RV5) of the ECG represents the left ventricular (LV) mass was investigated in 894 students aged 15 (boys: 545, girls: 349). The influence of body composition [ie, percentage of body fat (%fat)] was taken into consideration. A significant correlation was found between RV5 amplitude and LV mass for both genders. However, the relationship was stronger for boys than for girls. The students were then divided into 3 groups; that is, those at either the top or bottom 10th percentile (low or high-fat range) and the rest of the students (middle-fat range), depending on the % fat calculated by the bioelectrical impedance method. The significant correlation between RV5 and LV mass was found only for the 2 groups of boys whose percentage fat was in the low or middle-fat range. The correlation coefficients were 0.40 and 0.34, respectively. Moreover, in the boys' low-fat range, the RV5 of students whose LV mass was large (> or =90th percentile), was significantly higher (p<0.01) than in the other ranges. Setting a particular cutoff point of RV5 in the low-fat range of boys improved sensitivity as well as specificity (20-30% better among all boys) for detecting large LV mass. These observations suggest that classification of subjects by body composition could be improve the reliability of ECG assessment for left ventricular hypertrophy, although the gender and number of subjects in whom improvement is expected are limited.

Left Ventricular Morphology in Chronic Renal Failure by Echocardiography

M-mode, two-dimensional, and Doppler echocardiography were performed in 38 chronic renal failure (CRD) patients on conservative management, 35 patients on hemodialysis, and 36 matched controls. The controls were matched for age, sex, and comorbidities. The incidence of hypertension, left ventricular (LV) end diastolic volume, LV end systolic volume, and LV mass index were significantly higher in patients on hemodialysis compared to the controls. The LV parameters in the predialysis patients were not significantly different from the controls, except the LV end systolic internal dimensions were significantly higher in the CRF patients. Multiple regression analysis underscored the strong association between increase in LV mass index (LVMI) and hypertension. The diabetic patients with renal failure had large LV internal diameter and end diastolic volume compared to non-diabetics. Systolic function was well preserved even in hypertensive and diabetic patients with uremia. The incidence of diastolic dysfunction and asymmetrical septal hypertrophy were not significantly different in the three groups of patients.

Dispersion and delay of electrical restitution in the globally ischaemic heart

Alternans of action potential duration (APD) has been shown to be a precursor of ventricular fibrillation in ischaemic myocardium. We postulated that magnitude of alternans of APD during ischaemia depends not only on the severity of ischaemia but also on disturbed beat-to-beat restitution of APD. Monophasic action potentials were recorded simultaneously from right (RV) and left ventricular (LV) epicardial sites of isolated rabbit hearts. The inter-beat time courses of APD recovery were determined both during normal flow and ischaemia by interposing single cycle length changes ranging from 200 to 800 ms (= electrical restitution) simultaneously at the three recording sites. During normal perfusion, electrical restitution curves showed a steep initial recovery of APD, attaining steady-state values at extrastimulus cycle lengths of only 298 +/- 12 ms, with a high degree of uniformity between the three recording sites (inter-site variability < 2%). Ischaemia produced a marked slowing of electrical restitution which, on average, reached a plateau at extrastimulus cycle lengths of 415 +/- 45 ms, 650 +/- 72 ms and > 800 ms at 2 min, 5 min and 9 min of ischaemia, respectively (each P < 0.001 vs control). In addition, ischaemia resulted in a large inter-site variability, with RV and LV restitution curves deviating from each other by as much as 28.5% (P < 0.0001 vs baseline). We conclude that global ischaemia not only leads to a delayed but also non-uniform electrical restitution.(ABSTRACT TRUNCATED AT 250 WORDS)

Body surface distribution of abnormally low QRST areas in patients with left ventricular hypertrophy. An index of repolarization abnormalities.

QRST isointegral maps (I-maps) have been useful in detecting repolarization abnormalities. We investigated the body surface distribution of abnormally low QRST areas in patients with left ventricular hypertrophy (LVH) and the relation of the abnormalities in I-map to the severity of LVH as assessed by echocardiography. QRST area departure maps were constructed from electrocardiographic (ECG) data recorded in patients with LVH and precordial negative T waves resulting from aortic stenosis (AS) (10 patients), aortic regurgitation (AR) (12 patients), or hypertrophic cardiomyopathy (HCM) with asymmetric septal hypertrophy (22 patients). Fifty normal subjects served as controls. The I-map was constructed from 87 body surface electrocardiograms recorded simultaneously at a sampling interval of 1 msec. The area where the QRST area was smaller than normal limits (mean -2 SD) was designated the "-2 SD area." The echocardiographic left ventricular (LV) mass was calculated by Devereux's method. Patients with large LV masses due to AS or AR had 2 SD areas located over the left anterior chest or the midanterior chest, respectively. The 2 SD area was located over the left shoulder and left anterior chest and had a lingual shape in patients with HCM. The sum of QRST area values less than the normal range (sigma QRST) was significantly correlated with LV mass in patients with AS or AR (r = 0.83 and r = 0.69, p less than 0.01 and p less than 0.05). However, there was no significant correlation between sigma QRST and the severity of LVH in patients with HCM. sigma QRST divided by the number of electrodes in the 2 SD area was significantly greater in patients with HCM than in those with AS or AR. These findings suggest that abnormalities in patients with HCM are manifest even in mild LVH and that there is a greater disparity of repolarization in hypertrophied left ventricles due to HCM than in LVH due to aortic valve disease. QRST isointegral departure maps may provide ECG evidence of LV mass of patients with AS or AR and of susceptibility to malignant arrhythmias in patients with HCM.

Left ventricular pressure effects on right ventricular pressure and volume outflow

Massive destruction of the right ventricular free wall has been shown to cause only mild hemodynamic alterations. Further, the derivative of right ventricular (RV) pressure (P) is broad or double peaked, with one peak occurring coincidentally with peak left ventricular (LV) dP/dt. Both observations suggest a direct LV assistance to RV function. Since the ventricles contract nearly simultaneously, the relative contribution of LV to RV pump function has been difficult to determine. This LV assistance was quantified in six canine experiments using a unique electrically isolated RV preparation. While on total cardiopulmonary bypass, the RV free wall was electrically isolated from the remainder of the heart. This preparation allowed for wide variations in the timing interval between RV and LV contractions. Double-peaked waveforms for RVP and pulmonary flow (RVF) occurred over a wide range (0 to 300 ms) of pacing intervals between the RV and LV. One derivative peak always followed RV contraction for RVP and RVF (r = 0.971 +/- .011, P less than 0.01: r = 0.972 +/- .012, p less than 0.01; respectively). The second derivative peak was unrelated to the RA-RV pacing interval (r = 0.297 +/- .191, P greater than 0.5 RVP; 4 = 0.237 +/- .278, P greater than 0.5 RVF), but corresponded to the maximal LVP rise. Additionally, the magnitude of the two derivative peaks was similar when the ventricles contracted synchronously. When RV contraction preceded or followed LV contraction, the derivative peak associated with LV contraction was significantly greater (P less than 0.05, range 2.1 +/- 0.6 to 6.7 +/- 1.6 for RVP; P less than 0.05 range 1.9 +/- 0.4 to 6.7 +/- 1.5 for RVF) than the derivative associated with RV contraction. These data demonstrate a normally present, large LV assistance to RV contraction and may help to explain the RV response to myocardial infarction.

Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall.

Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 +/- 0.6 ml), middle (15.3 +/- 1.0 ml), and large (20.5 +/- 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 +/- 0.13, 2.74 +/- 0.13, and 2.89 +/- 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p less than 0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 +/- 0.68, 3.39 +/- 0.67, and 2.87 +/- 0.71 ml, respectively; p less than 0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 +/- 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 +/- 0.55, 9.81 +/- 0.56, and 9.92 +/- 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)