Impaired Left Ventricular Performance Research Articles

ECG Changes in a 25-Year-Old Woman With Hypocalcemia Due to Hypoparathyroidism: Hypocalcemia Mimicking Acute Myocardial Infarction

The case of a 25-year-old woman presenting with chest pain, ECG changes, and laboratory findings suggestive of myocardial infarction is reported. Cardiac catheterization showed impaired left ventricular performance but otherwise normal coronary arteries. Laboratory analyses revealed primary hypoparathyroidism, and supplementation with calcium and vitamin D(3) was initiated. There was subsequent improvement in laboratory findings as well as echocardiographically determined left ventricular performance. Thereafter, the patient remained asymptomatic. Apart from some persisting ECG repolarization disturbances, there was complete normalization of the initial changes. This case demonstrates a combination of clinical, blood biochemical, and ECG findings mimicking acute myocardial infarction.

Carotid artery disease as a marker for the presence of severe coronary artery disease in patients evaluated for chest pain.

We sought in this study to elucidate whether carotid artery disease detected by ultrasonography can be a clinically useful marker for the presence of severe coronary artery disease (CAD) in patients evaluated for chest pain. Duplex ultrasonography and quantitative coronary angiography were used to assess carotid and coronary artery atherosclerosis in 225 consecutive patients (mean age, 58+/-9 years) with chest pain referred for cardiac catheterization. CAD was present in 197 patients (88%). Fifty-seven patients (25%) had 1-vessel disease, 52 (23%) had 2-vessel disease, 53 (24%) had 3-vessel disease, and 35 (16%) had left main stem CAD (LMS-CAD). The incidence of severe CAD (3-vessel disease or LMS-CAD) was 24% and 63% in the normal and impaired ejection fraction (EF) subgroups, respectively (P<0.005). Carotid disease (lumen diameter stenosis of >/=50%) was present in 5.3%, 13.5%, 24.5%, and 40% of patients with 1-, 2-, and 3-vessel disease and LMS-CAD, respectively. Moreover, the incidence of carotid disease in patients with severe CAD was 31% in the entire study population and 46% and 5% in the subgroups with impaired and normal EF, respectively (P<0.005). In the entire study population, the presence of severe CAD was determined by age, male sex, and carotid disease; in the impaired EF group by age and carotid disease; and in the normal EF group only by age. Carotid disease has a high negative (92%) and a high positive (91%) predictive value for the presence of severe CAD in the subgroup with normal and impaired EF, respectively. In patients evaluated for chest pain, carotid disease is significantly correlated with severe CAD. Furthermore, in patients with impaired left ventricular systolic performance the presence of carotid disease reflects the presence of severe CAD, while in patients with normal EF the absence of carotid disease reflects the absence of severe CAD.

Myocardial injury and left ventricular performance after subarachnoid hemorrhage.

Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (n=67) or on the day of echocardiography (n=5) if surgery was not performed (mean, 3. 3+/-1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB <1%, n=36), mild (peak CK-MB 1% to 2%, n=21), moderate (peak CK-MB >2%, n=6), or severe (abnormal left ventricular wall motion, n=9). Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels >2% (P<0.0001), poor neurological grade (P=0.002), and female sex (P=0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels <1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both P<0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (P<0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval [95% CI], 1.0 to 3.4; P=0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; P=0.04) were independent predictors of symptomatic vasospasm. Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm.

Contraction-relaxation coupling and impaired left ventricular performance in coronary surgery patients.

Dependence of left ventricular (LV) relaxation on cardiac systolic load is a function of myocardial contractility. The authors hypothesized that, if a tight coupling would exist between LV contraction and relaxation, the changes in relaxation rate with an increase in cardiac systolic load would be related to the changes in LV contraction. Coronary surgery patients (n = 120) with preoperative ejection fraction >40% were included. High-fidelity LV pressure tracings (n = 120) and transgastric transesophageal echocardiographic data (n = 40) were obtained. Hearts were paced at a fixed rate of 90 beats/min. Effects on contraction were evaluated by analysis of changes in dP/dt(max) and stroke area. Effects on relaxation were assessed by analysis of R (slope of the relation between tau and end-systolic pressure). Correlations were calculated with linear regression analysis using Pearson's coefficient r. Baseline LV end-diastolic pressure was 10+/-3 mm Hg (mean +/- SD). During leg raising, systolic LV pressure increased from 93+/-9 to 107+/-11 mm Hg. The change in dP/dt(max) was variable and ranged from -181 to +254 mm Hg/s. A similar variability was observed with the changes in stroke area, which ranged from -2.0 to +5.5 cm2. Changes in dP/dt(max) and in stroke area were closely related to individual R values (r = 0.87, P<0.001; and r = 0.81, P<0.001, respectively) and to corresponding changes in LV end-diastolic pressure (r = 0.81, P< 0.001; and r = 0.74, P<0.001, respectively). A tight coupling was observed between contraction and relaxation. Leg raising identified patients who developed a load-dependent impairment of LV performance and increased load dependence of LV relaxation.

Low incidence of significant valvar insufficiency following retrograde aortic radiofrequency catheter ablation in young patients.

The incidence of significant valvar insufficiency at late (<6 month) follow-up was retrospectively evaluated in 27 young patients (age 4. 0-18.0 years) undergoing 29 ablation procedures via the retrograde aortic approach for left-sided accessory connections in whom pre-ablation and post-ablation echocardiograms were available for review. Valvar insufficiency was graded using color flow techniques as absent, trivial, mild, moderate, or severe by blinded reviewers. Ablation was acutely successful via the retrograde approach in 25 of 29 procedures among these 27 patients. Successful ablation was ultimately achieved in all 27 patients. At baseline, 7 patients had evidence of trivial or mild mitral insufficiency, and no patient had aortic insufficiency. Three patients had evidence of impaired left ventricular systolic performance in the presence of manifest pre-excitation. At follow-up, pre-existing mitral insufficiency resolved in 5/7 patients, and persisted in 2 patients. New mitral insufficiency was evident in 3 patients, and new aortic insufficiency was transiently evident in 1 patient following ablation (all trivial). Institutional experience (mean rank 10 cases vs. 33 cases, p <.0005), and lower patient weight (29.7 vs. 56.3 kilograms, p =.01) were the only factors associated with the development of new valvar insufficiency. Valvar insufficiency could not be detected by careful auscultation in any patient and was deemed clinically insignificant in all patients. We conclude that ablation of left-sided accessory connections can be performed via the retrograde aortic approach without creating clinically significant valvar insufficiency.

Changes of left ventricular function after percutaneous balloon mitral valvuloplasty in mitral stenosis with impaired left ventricular performance

The pathophysiological role of mechanical and myocardial factors for impairment of left ventricular performance in mitral stenosis is still not clear. To investigate this controversy, 27 patients of mitral stenosis with left ventricular ejection fraction <50% were studied. Patients were divided into two groups: Group 1: 20 patients, left ventricular ejection fraction improved to >50% after valvuloplasty, and Group 2: 7 patients, left ventricular ejection fraction still <50% after valvuloplasty. The clinical and hemodynamic characteristics were comparable for the two groups before valvuloplasty. Follow-up catheterization done one week later showed similar changes in mitral valve area, cardiac index, pulmonary pressure, left ventricular end-diastolic volume index and systemic vascular resistance between the two groups. However, left ventricular end-systolic volume was significantly decreased after valvuloplasty in Group 1 but not in Group 2, resulting in significantly higher ejection fraction in Group 1 than in Group 2. Postoperatively, regional wall motion scores were lower in Group 1 than in Group 2 (2.0 ± 0.6 vs. 2.7 ± 0.5 at the anterolateral wall, P = 0.002; 1.9 ± 0.6 vs. 2.9 ± 0.4 at the posterobasal wall, P = 0.0003). Most of our mitral stenosis patients with impaired left ventricular ejection fraction showed improvement after mitral valvuloplasty had released the mechanical obstruction. However, in some patients, impaired ejection fraction persisted after valvuloplasty, suggesting the mechanism of myocardial failure. Thus, both myocardial and mechanical factors play important roles in the pathogenesis of left ventricular ejection performance impairment.

Changes of left ventricular function after percutaneous balloon mitral valvuloplasty in mitral stenosis with impaired left ventricular performance

<h2>Abstract</h2> The pathophysiological role of mechanical and myocardial factors for impairment of left ventricular performance in mitral stenosis is still not clear. To investigate this controversy, 27 patients of mitral stenosis with left ventricular ejection fraction <50% were studied. Patients were divided into two groups: Group 1: 20 patients, left ventricular ejection fraction improved to >50% after valvuloplasty, and Group 2: 7 patients, left ventricular ejection fraction still <50% after valvuloplasty. The clinical and hemodynamic characteristics were comparable for the two groups before valvuloplasty. Follow-up catheterization done one week later showed similar changes in mitral valve area, cardiac index, pulmonary pressure, left ventricular end-diastolic volume index and systemic vascular resistance between the two groups. However, left ventricular end-systolic volume was significantly decreased after valvuloplasty in Group 1 but not in Group 2, resulting in significantly higher ejection fraction in Group 1 than in Group 2. Postoperatively, regional wall motion scores were lower in Group 1 than in Group 2 (2.0 ± 0.6 vs. 2.7 ± 0.5 at the anterolateral wall, <i>P</i> = 0.002; 1.9 ± 0.6 vs. 2.9 ± 0.4 at the posterobasal wall, <i>P</i> = 0.0003). Most of our mitral stenosis patients with impaired left ventricular ejection fraction showed improvement after mitral valvuloplasty had released the mechanical obstruction. However, in some patients, impaired ejection fraction persisted after valvuloplasty, suggesting the mechanism of myocardial failure. Thus, both myocardial and mechanical factors play important roles in the pathogenesis of left ventricular ejection performance impairment.

Congestive Heart Failure Due to Reversible Cardiomyopathy in Patients With Hyperthyroidism

The authors describe the clinical characteristics and response to therapy of seven patients with hyperthyroidism, dilated cardiomyopathy, and low-output cardiac failure. All patients (4 women and 3 men, age 47 +/- 4 years, mean +/- standard error of the mean) were admitted with the primary diagnosis of congestive heart failure. The cause of hyperthyroidism was Graves' disease in six patients, and toxic multinodular goiter in one. On admission, the mean serum T4 was 21 +/- 1 microgram/dL and mean serum T3:411 +/- 77 ng/mL, and serum thyroid-stimulating hormone was suppressed ( < 0.03 microU/mL) in all patients. Two-dimensional echocardiogram showed biventricular or four chamber dilatation and impaired left ventricular performance. Therapy of heart failure and hyperthyroidism resulted in rapid clinical improvement. During follow-up (5 months to 9 years), left ventricular ejection fraction improved from a mean of 28% to a mean ejection fraction of 55% (P < 0.01). Resolution of dilated cardiomyopathy with normalization of systolic function was achieved in five patients, and improvement from severe to mild left ventricular dysfunction was observed in two patients. We conclude that some patients with hyperthyroidism may have a reversible form of dilated cardiomyopathy and "low-output failure." Assessment of thyroid hormone status in patients with heart failure might permit the identification of patients with dilated cardiomyopathy and thyrotoxicosis who are likely to have reversible cardia dysfunction.

Structural Basis for Heart Failure

The syndrome of heart failure has traditionally been viewed as a functional disorder precipitated by impaired left ventricular pump performance. The classification into systolic and diastolic dysfunction has emphasized the functional distinction between abnormalities in contraction and relaxation. Recently, however, attention has been directed toward the possibility that the systolic dysfunction, which has been thought to be related to contractile failure, could be a consequence of a structural increase in ventricular chamber volume. This construct would revise the conventional view—contractile failure leads to chamber dilatation—with a more anatomic basis for heart failure: Chamber dilatation occurs as an early response that results in the reduced wall motion that is mandated to generate a normal stroke volume from a large ventricular end-diastolic volume. This structural alteration is not necessarily related to the underlying etiological cardiac pathology but rather represents an intrinsic morphological change that progresses over time in response to an initiating event. The term “remodeling” often is used to address these structural changes and may be best defined as a change in chamber volume and shape not related to a preload-mediated increase in sarcomere length. In this issue of Circulation , Greenberg and his SOLVD colleagues1 revisit the remodeling issue in chronic heart failure with echocardiographic data collected in the long-term trial of enalapril versus placebo in both symptomatic and asymptomatic patients with left ventricular remodeling. Patients were selected for this study on the basis of an ejection fraction of ≤35%. At the time the study was designed, this low ejection fraction was defined as systolic dysfunction. The implication of that designation is that an impairment of myocardial shortening was the primary abnormality. A more contemporary hypothesis, based on the concept of left ventricular remodeling, is that the low ejection fraction reflects in part a primary increase in chamber volume …

Long-term outcome in patients with congestive heart failure and intact systolic left ventricular performance

Congestive heart failure (CHF) is typically associated with impaired left ventricular (LV) systolic performance. Few reports exist describing the long-term outcome in patients with CHF and normal LV systolic function. Fifty-two patients initially hospitalized with CHF and intact LV function (ejection fraction ≥45%) were followed for 7 years. Mean age when initially identified was 71 ± 11 years (range 36 to 96), and average LV ejection fraction was 61 ± 11%. CHF was graded by a clinicoradiographic index, with a mean of 7.0 ± 2.3 (range 3 to 12, 13 indicates worst CHF). A third heart sound was present in 19 patients (37%), and 17 (33%) had presented with acute pulmonary edema. Principal cardiovascular diagnoses were coronary artery disease in 27 (52%), hypertensive heart disease in 16 (31%) and restrictive cardiomyopathy in 7 (13%). At 7 years, cardiovascular mortality was 46% (24 of 52), and noncardiovascular mortality was 10% (5 of 52). Survival was not correlated with age, principal diagnosis, third heart sound, pulmonary edema at presentation, LV ejection fraction, or presence or degree of LV diastolic dysfunction. Cardiovascular morbidity, consisting of nonfatal recurrent CHF, myocardial infarction, unstable angina or other cardiovascular events occurred in 29% (15 of 52). Combined cardiovascular mortality and morbidity was 75% (39 of 52). In patients with CHF, intact LV systolic function does not confer the same favorable prognosis it defines in other clinical situations. For such patients, the risk of future cardiovascular events is high, a finding that should be considered when designing therapeutic strategies in this group.

Mechanisms of exercise limitation in hypertrophic cardiomyopathy

To assess the relation of exercise capacity to indexes of systolic and diastolic function in hypertrophic cardiomyopathy, 81 patients underwent two-dimensional echocardiography, technetium-99m equilibrium radionuclide angiography acquired in list mode and maximal, symptom-limited, treadmill exercise testing with measurement of maximal oxygen consumption (VO2 max). VO2 max for the group was 13.9 to 49.3 (mean 25.4) ml/min per kg. Thirty-six patients (44%) achieved less than or equal to 70% of age-predicted VO2 max. Patients with such a degree of limitation were more likely to be in New York Heart Association functional class II or III (23 of 36 vs. 14 of 45; p = 0.005); there was no such relation between VO2 and the incidence and magnitude of rest left ventricular outflow tract pressure gradient greater than 30 mm Hg (11 of 36 vs. 11 of 45; p = NS and 58 +/- 24 vs. 65 +/- 19 mm Hg; p = NS). In the 22 patients with a left ventricular outflow tract gradient, the ratios of peak ejection to peak filling rate and of atrial contribution to left atrial dimension were related to percent of the age-predicted VO2 max (r = 0.49, p = 0.02 and r = 0.54, p less than 0.02). These ratios reflect impaired left ventricular systolic performance and atrial systolic failure, respectively. Stepwise discriminant analysis revealed these two ratios to be the two strongest predictors (p = 0.0001) of patients with a left ventricular outflow tract gradient whose VO2 max was less than or equal to 70% of the age-predicted value (sensitivity 90%, specificity 100%).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular ejection performance in mitral stenosis, and effects of successful percutaneous transvenous mitral commissurotomy

Impaired left ventricular ejection performance was reported in pure mitral stenosis. The speculative mechanisms included insufficient preload, increased wall stress, high right ventricular pressure and unknown myocardial factors, but no definitive mechanism has been established. Fifteen patients with tight mitral stenosis who underwent successful percutaneous transvenous mitral commissurotomy were studied to ascertain whether ejection performance would improve with sufficient blood filling. The indexes of preload (end-diastolic volume) and ejection performance (stroke volume, ejection fraction, and mean systolic and mean normalized ejection rates) were calculated angiographically before and immediately after mitral commissurotomy. Improved blood filling (the result of successful mitral commissurotomy) produced an increase in end-diastolic volume (mean ± SD 99.0 ± 30.2 to 112.1 ± 30.1 ml/m 2; p < 0.05). All 4 indexes of ejection performance also improved. There was good correlation between end-diastolic and stroke volumes before intervention (stroke volume = 0.476 × end-diastolic volume + 16.77; r = 0.76), and the relation between them showed no change even after mitral commissurotomy. It is concluded that both left ventricular preload and ejection performance improved after successful percutaneous transvenous mitral commissurotomy. Insufficient preload could affect ejection performance in patients with tight mitral stenosis.

Influence of pre-existing ischemia on recovery from chemical cardioplegia. A study on pig hearts in an isolated blood-perfused model.

The impact of prior cardiac ischemia on recovery from chemical cardioplegia was investigated in pig hearts. Group I hearts were subjected to 9-min normothermic ischemia before the start of chemical cardioplegia. After 180 min of induced cardiac arrest, all hearts were reperfused and monitored for 120 min in a blood-perfused Langendorff model. Consistent with left ventricular performance, myocardial oxygen uptake was significantly lower in group I than in the other hearts during the first 60 min of reperfusion. Lactate elimination was significantly higher in group I at the start of reperfusion, but showed no intergroup difference after 25 min. Nor was intergroup difference found in left ventricular end-diastolic pressure, total myocardial flow or glucose extraction fraction during reperfusion. The mitochondrial ultrastructure was identical in the two groups before chemical cardioplegia. During cardioplegia it deteriorated in group I but normalized in group II. During reperfusion these circumstances were reversed. Although precardioplegic ischemia thus significantly impaired left ventricular performance during early recovery, with corresponding effects on metabolism and ultrastructure, stable performance during reperfusion indicated that the ischemic injury did not worsen.

Relation between cyclic variation in echo amplitude and segmental contraction in normal and abnormal hearts.

To study the relation between cardiac systolic activity and cardiac cycle dependent variation in the ultrasound signal arising from within the myocardium. Regional echo amplitude was used as a measure of the myocardial ultrasound signal. Relative echo amplitude values were assigned by standardising echo gain using the posterior parietal pericardium as an in-vivo calibration. M mode measurements of the left ventricle were used to assess cardiac systolic activity. Subjects were studied prospectively. Analysis of echo amplitude was performed by investigators who were blinded to the results of the M mode analysis. The influence of impaired left ventricular performance and abnormal wall motion were assessed. 11 cardiomyopathy patients with impaired ventricular function, eight patients with severe pulmonary hypertension and reversed septal motion, and 19 healthy controls. All subject studies were performed at Harefield Hospital. Echo amplitude analysis was performed at the Royal Brompton Hospital. Cyclic variation in echo amplitude was determined as the change in echo amplitude from end diastole to end systole. Additionally, an index of cyclic variation defined as the ratio of the cyclic change in echo amplitude to end diastolic echo amplitude was measured. Both cyclic variation and the cyclic variation index were analysed to see whether they correlated with left ventricular dimensions, fractional shortening, and systolic wall thickening. Stepwise regression analysis showed systolic wall thickening to be the most significant independent variable that correlated with the cyclic variation index for both the septum and posterior wall (r = 0.68, p = 0.0001, septum; r = 0.69, p = 0.0001, posterior wall). The slopes and intercepts for both regression equations were similar (y = 0.005x + 0.006, septum; y = 0.006x + 0, posterior wall). Subgroup analysis showed that the healthy controls, patients with cardiomyopathy, and patients with pulmonary hypertension had similar slopes and intercepts for their individual regression equations. These data support the hypothesis of a quantitative relation between the extent of cyclic variation of echo amplitude and the degree of segmental myocardial shortening, as measured by systolic wall thickening, which is not significantly influenced by location within the myocardium, left ventricular performance, or wall motion. They provide further evidence of the usefulness of quantitative analysis of myocardial echo amplitude in the study of regional myocardial function in both normal and injured myocardium.

Noncoordinate regulation of alpha-1 adrenoreceptor coupling and reexpression of alpha skeletal actin in myocardial infarction-induced left ventricular failure in rats.

To determine the effects of myocardial infarction-induced left ventricular failure on the regulation of surface alpha-1 adrenoreceptors and signal transduction, large infarcts were produced in rats and the animals killed seven days later. After the documentation of impaired left ventricular pump performance, radioligand binding studies of the alpha-1 adrenoreceptor, norepinephrine-stimulated phosphoinositol turnover, and ADP ribosylation of 41 kD substrate by pertussis toxin were examined in the hypertrophying unaffected myocardium. Moreover, the expression of sarcomeric actin isoforms was analyzed by Northern blots and hybridization with specific oligonucleotide probes. Alpha-1 adrenoreceptor density was found not to be altered in membranes obtained from the spared left ventricular tissue, whereas phosphoinositol turnover was increased 3.1-fold in the viable myocytes of infarcted hearts. Furthermore, pertussis toxin substrate was augmented 2.5-fold in membranes prepared from the surviving left ventricular myocardium. Finally, an upregulation of the skeletal actin isoform was detected in the tissue of the failing left ventricle. In conclusion, the possibility is raised that in the presence of severe myocardial dysfunction and ongoing reactive hypertrophy, effector pathways linked to the alpha-1 adrenoreceptor may stimulate the myocyte hypertrophic response which would tend to normalize cardiac hemodynamics. The reexpression of alpha skeletal actin may be a molecular indicator of the persistance of an overload on the myocardium.

Mild mitral insufficiency is a marker of impaired left ventricular performance in aortic stenosis

Whether mitral insufficiency is a marker of decreased left ventricular function in patients undergoing aortic valve replacement for severe aortic stenosis was examined. Hemodynamic measurements in 26 patients with pure aortic stenosis (Group 1), 17 patients with aortic stenosis and grade 1 or 2 mitral insufficiency (Group 2) and 19 control patients were compared. All patients were free of significant coronary artery disease. Ventriculograms were digitized for calculation of ejection fraction, ventricular volumes and wall stress.Despite similar aortic valve areas, Group 2 patients had more advanced symptoms. Cardiac index was comparably decreased in Group 1 (2.6 ± 0.4 liters/min per m2) and Group 2 (2.7 ± 0.8 liters/min per m2) compared with the control group (3.8 ± 0.6 liters/min per m2). Left ventricular end-diastolic and end-systolic volume indexes were increased only in Group 2 (119 ± 35 and 73 ± 36 ml/m2, respectively). Likewise, end-systolic wall stress was increased only in Group 2 (149 ± 54 kdynes/cm2). Ejection fraction was decreased to a greater extent in Group 2 (42 ± 17%) than in Group 1(59 ± 13%) as compared with values in the control group (68 ± 5%). Although an inverse relation existed between ejection fraction and end-systolic stress in all groups, the ejection fraction (extrapolated to end-systolic stress = 0) was decreased in Group 2, and the slope of the relation was increased in Groups 1 and 2. The end-systolic stress/end-systolic volume index ratio, an index of ventricular performance, was also decreased to a greater extent in Group 2.In severe aortic stenosis, the presence of mild mitral insufficiency is a marker of decreased contractile performance and may affect the perioperative and long-term prognosis.

Electrocardiographic markers of impaired left ventricular ejection performance in aortic stenosis

To determine whether the ECG would be useful in the prediction of impaired left ventricular ejection performance in aortic valve stenosis, the authors evaluated 121 patients according to (1) the time relationship of the R peak in V 6 to the S peak in V 2 ; and (2) the negative P wave terminal force in V 1 (Morris index, n = 109). Left ventricular ejection fraction (LVEF) was significantly depressed in patients with the R peak in V 6 later than the S peak in V 2 (R peak delay in V 6 , n = 24), compared with those with the R peak in V 6 preceding the S peak in V 2 or with both peaks occurring simultaneously (n = 97) (LVEF 40.8 ± 11.8% vs 69.9 ± 13.3%, p = .000). LVEF < 55% was present in 87.5% of patients with the R peak delay in V 6 and in only 23.7% of those without this finding. The Morris Index was significantly greater in patients with LVEF < 55% (n = 39) than in those with LVEF ≥ 55% (n = 70) (Morris Index 0.063 ± 0.035 msec vs 0.030 ± 0.025 msec, p = .000). The R peak delay in V 6 is a highly specific (96.1%), but less sensitive (47.7%), indicator of depressed LVEF, its positive predictive value and predictive accuracy being 87.5% and 78.5%, respectively. Of the Morris indexes, only ≥ 0.06 msec (n = 28) indicates that depressed LVEF (< 55%) is nearly as reliable as the R peak delay in V 6 (sensitivity, 51.7%; specificity, 88.5%; positive predictive value, 75.6%; predictive accuracy, 73.5%). Thus, the criteria are useful indicators of reduced LVEF, which could reflect either abnormally high systolic wall stress or decreased myocardial contractility.

Electrocardiographic markers of impaired left ventricular ejection performance in aortic stenosis

To determine whether the ECG would be useful in the prediction of impaired left ventricular ejection performance in aortic valve stenosis, the authors evaluated 121 patients according to (1) the time relationship of the R peak in V 6 to the S peak in V 2; and (2) the negative P wave terminal force in V 1 (Morris index, n = 109). Left ventricular ejection fraction (LVEF) was significantly depressed in patients with the R peak in V 6 later than the S peak in V 2 (R peak delay in V 6, n = 24), compared with those with the R peak in V 6 preceding the S peak in V 2 or with both peaks occurring simultaneously (n = 97) (LVEF 40.8 ± 11.8% vs 69.9 ± 13.3%, p = .000). LVEF < 55% was present in 87.5% of patients with the R peak delay in V 6 and in only 23.7% of those without this finding. The Morris Index was significantly greater in patients with LVEF < 55% (n = 39) than in those with LVEF ≥ 55% (n = 70) (Morris Index 0.063 ± 0.035 msec vs 0.030 ± 0.025 msec, p = .000). The R peak delay in V 6 is a highly specific (96.1%), but less sensitive (47.7%), indicator of depressed LVEF, its positive predictive value and predictive accuracy being 87.5% and 78.5%, respectively. Of the Morris indexes, only ≥ 0.06 msec (n = 28) indicates that depressed LVEF (< 55%) is nearly as reliable as the R peak delay in V 6 (sensitivity, 51.7%; specificity, 88.5%; positive predictive value, 75.6%; predictive accuracy, 73.5%). Thus, the criteria are useful indicators of reduced LVEF, which could reflect either abnormally high systolic wall stress or decreased myocardial contractility.

Beneficial effects of coenzyme Q10 on impaired left ventricular performance in streptozotocin diabetic rats.

Chronic effects of coenzyme Q10 (CoQ: 30 mg/kg/day for 12 weeks) on cardiac performance in streptozotocin (45 mg/kg) induced diabetic rats were examined. Cardiac performance was assessed using the isolated retrograde perfused isovolumically contracting heart model. Compared to age matched nondiabetic rats, decreases occurred in myocardial CoQ (25.8 +/- 3.3 vs. 31.9 +/- 2.7 micrograms/ml), AMP (0.9 +/- 0.7 vs. 2.0 +/- 0.4 micrograms/mg), Emax (37 +/- 14 vs. 80 +/- 38 mmHg/microliter/g), an index of myocardial contractility, and LV diastolic chamber stiffness constant k (0.68 +/- 0.13 vs. 1.31 +/- 0.59 g/microliter) in diabetic rats. Normalized left ventricular weight (2.97 +/- 0.23 vs. 2.51 +/- 0.21 mg/g) and volume (1.53 +/- 0.34 vs. 0.89 +/- 0.53 microliter/g) and time constant of left ventricular pressure fall, T (32.0 +/- 8.0 vs. 19.7 +/- 2.6 ms) increased in diabetes. In diabetic rats taking CoQ, myocardial CoQ (28.5 +/- 3.2 micrograms/ml) and AMP (2.1 +/- 1.7 micrograms/mg) were the same as control, and T (23.5 +/- 7.4 ms) was significantly shortened (mean +/- SD, p less than 0.05, p less than 0.01). To compensate for depressed myocardial contractility and relaxation, LV dilatation and increased LV mass occurred in diabetic rats. Exogenous CoQ increased myocardial CoQ content and improved myocardial relaxation in diabetic rats.

Increased mortality of diabetics after acute myocardial infarction attributed to diffusely impaired left ventricular performance as assessed by echocardiography.

Five hundred and forty-eight patients who sustained their first acute myocardial infarction (AMI) were admitted to the coronary care unit (CCU). Ninety-eight of them were known diabetics. The diabetic patients were younger, 50 +/- 12 vs. 64 +/- 18 years of age (p less than 0.05), and the proportion of females in their group was higher than in the nondiabetics, 44% vs. 33.4% (p less than 0.05). The in hospital mortality rate was 30% for diabetics and 16% for nondiabetics (p less than 0.001). Diabetics had a higher percentage of mortality caused by left ventricular failure (LVF) (p less than 0.025) and a tendency for more frequent complete A-V block (p less than 0.01) compared to nondiabetics. Obesity and a positive family history for coronary heart disease were more prevalent in the diabetic group (both p less than 0.01). The echocardiographic assessment of left ventricular function, performed in 125 consecutively admitted patients (25 diabetics and 100 nondiabetics) on the 3rd-5th post-infarct day, showed that the indices of myocardial contractility, that is, E point septal separation (EPSS), ejection fraction (EF) and fractional shortening (FS) were far more impaired in diabetics than in nondiabetics (p less than 0.01, p less than 0.005, p less than 0.005, respectively). No significant difference was found in the prevalence of dyskinetic, akinetic and hypokinetic segments between the two categories of patients, suggesting no difference in the amount of myocardial mass affected by the AMI. Our results indicate that the increased incidence of LVF developed in diabetics after an AMI compared to nondiabetics may be caused by other factors, probably some form of latent diabetic cardiomyopathy as a result of either small vessel disease or metabolic disorder.