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Myocarditis in beta-thalassemia major. A cause of heart failure.

BACKGROUND: Although acute pericarditis is a common complication of beta-thalassemia major, the prevalence and consequences of myocarditis in this disease have not been investigated. METHODS AND RESULTS: A prospective 5-year follow-up study was carried out in all patients with beta-thalassemia major in whom the diagnosis of acute infectious myocarditis could be established between 1977 and 1986. A similar number of age- and sex-matched control subjects with beta-thalassemia and normal left ventricular function and no evidence of myocarditis were also followed for 5 years. Of 1048 patients with beta-thalassemia major, 47 patients (age, 15 +/- 2.5 years) with precordial chest pain were diagnosed as having acute infectious myocarditis. Myocardial biopsy was diagnostic in 26 patients, border-line in 14 patients, and nondiagnostic in 7 patients. Acute heart failure with left ventricular dysfunction (left ventricular ejection fraction, 25 +/- 11%) developed in 11 patients (23.4%) with myocarditis, and 8 of them died within 1 month to 1 year after diagnosis. Thirteen patients with myocarditis (27.6%) developed chronic heart failure (left ventricular ejection fraction, 26 +/- 13%) within 3 +/- 1.3 years, and 10 of them died within 8 +/- 3 months. Left ventricular systolic and diastolic functions of the control subjects did not change significantly during the 5-year period (left ventricular ejection fraction, 63 +/- 11% versus 65 +/- 7%; P = NS). However, left ventricular restrictive abnormalities (early diastole/late diastole, > 2.2; deceleration time, < 110 milliseconds) combined with right ventricular dilatation (> 30 mm internal diameter) and right-sided heart failure developed in 3 patients with extremely high mean serum ferritin levels. No significant difference was found in mean levels of serum ferritin and pretransfusion hemoglobin between patients with and those without myocarditis. CONCLUSIONS: In patients with beta-thalassemia, myocarditis appears to be involved in the pathogenesis of left ventricular systolic dysfunction, being the main cause of death. Iron overload appears to provoke left ventricular restrictive abnormalities combined with right ventricular enlargement and dysfunction.

Adolescent↗

Increased dependence on slow filling for left ventricular diastolic filling in patients with coronary artery disease and a depressed systolic function--assessment with radionuclide ventriculography.

Contributions of rapid filling, slow filling and atrial systole to the left ventricular (LV) filling volume were analyzed with the use of radionuclide ventriculography at rest, both globally and regionally, in 34 patients with isolated disease of the left anterior descending coronary artery. The patients included 17 with a normal ejection fraction (EF greater than or equal to 50%; group 1) and 17 with a depressed EF (less than 50%; group 2), and the data were compared with those obtained from 13 normal subjects. A computer program subdivided the LV image into 4 regions, and time-activity curves were constructed globally and regionally by reverse-gating from the R wave. In both groups the contribution of rapid filling to the LV filling volume was decreased significantly in the affected septal and apical regions, and in the global left ventricle compared with that in normal subjects. In group 1, the contribution of atrial systole showed an increase in these affected regions and in the global left ventricle. In contrast, in group 2, the atrial contribution was not increased globally or regionally as much as was expected. However, the contribution of slow filling was either increased significantly or tended to increase in the affected regions and in the global left ventricle. There were negative correlations between the contribution of rapid filling and that of slow filling in the global left ventricle (r = -0.73, p less than 0.001) and in each of the septal, apical and lateral regions (r greater than or equal to -0.60, p less than 0.001), which suggested that the contribution of slow filling as well as of atrial systole undergoes an increase as rapid filling is impaired. Thus, in patients with coronary artery disease, the left ventricle relies on slow filling as well as atrial systole to affect diastolic LV filling in the affected regions and in the global left ventricle in the presence of LV systolic dysfunction.

Adult↗

Thrombi in left ventricular hypertrabeculation/noncompaction--review of the literature.

OBJECTIVE: Left ventricular hypertrabeculation/noncompaction (LVHT) is diagnosed when numerous, excessively prominent trabeculations and deep interventricular recesses are found in the left ventricle. Although it is assumed that the intertrabecular recesses are a location prone to thrombus formation, the prevalence of thrombi in LVHT hearts is unknown. METHODS: A Medline research was carried out looking for reports of pathoanatomical investigations of LVHT hearts. Excluded were reports in which a connection between the coronary arteries with the intertrabecular recesses were described. RESULTS: In 22 articles pathoanatomical findings of 37 hearts were described (9 women, 27 men, 1 not indicated). The age ranged from 26 gestational weeks to 80 years. Twenty-four hearts were investigated by autopsy, 13 as explanted hearts. The left ventricle was dilated in 29 patients. In 9 patients, a previous embolic event had occurred. All 9 patients had additional risk factors for embolism such as atrial fibrillation (n = 1), left ventricular dysfunction (n = 5) or atrial fibrillation and left ventricular dysfunction (n = 3). In only 2 patients, a thrombus was detected pathoanatomically. CONCLUSIONS: Thrombus-formation is a rare event in patients with LVHT. From these data we infer that LVHT in itself is no indication for oral anticoagulation. However, if additional cardiac abnormalities, known to increase the risk of embolism, like atrial fibrillation or left ventricular systolic dysfunction, accompany LVHT, they have to be treated as usual.

Autopsy↗

[Elderly heart failure patients and the role of beta-blocker therapy].

In this article different aspects of chronic heart failure in old age are described. We mainly focus on the place of beta-blocker therapy in chronic heart failure. Beta-blockers are recommended for the treatment of stable chronic heart failure with left ventricular systolic dysfunction. There is additional information from recent studies that there is proven efficacy for beta-blocker therapy in patients with heart failure up to the age of 80 years. For patients with heart failure aged 80 and over the evidence to prescribe beta-blockers is limited. However, it is known that also in very elderly patients beta-blocker therapy is well tolerated. In patients with heart failure with preserved systolic ventricular function there is still no evidence that there is a beneficial effect of beta-blockers. It is still not clear if there are differences between beta-blocking agents. Of all beta-blockers, only bisoprolol, carvedilol, nebivolol and metoprolol CR are proven effective in stable chronic heart failure with impaired left ventricular systolic function and can be recommended in elderly patients on standard treatment with diuretics and ACE inhibition.

Adrenergic beta-Antagonists↗

Left atrial myopathy in idiopathic dilated cardiomyopathy.

To investigate whether left atrial systolic dysfunction in dilated cardiomyopathy is the result of left atrial dilatation, atrial involvement in the myopathic process, or both, 20 patients with aortic stenosis, 14 patients with idiopathic dilated cardiomyopathy, and 10 normal control subjects were studied. Left atrial volumes (cubic centimeters) were echocardiographically measured at mitral valve opening (maximal), mitral valve closure (minimal), and onset of atrial systole (P wave of the electrocardiogram) with the biplane area-length method. Atrial systolic function was assessed by calculating the active emptying fraction, equal to (volume at onset of atrial systole minus minimal volume)/volume at onset of atrial systole. Heart rate was similar in patients with aortic stenosis and dilated cardiomyopathy (83 +/- 11 vs 86 +/- 15 beats/min, respectively). Maximal volume was similar in patients with aortic stenosis (74.8 +/- 26.4 cm3) and dilated cardiomyopathy (79.7 +/- 25.3 cm3) but greater (p < 0.0001) than in control subjects (46.4 +/- 11.9 cm3). Active emptying fraction was inversely related to volume at onset of atrial systole and to tension at end of atrial systole (aortic stenosis r = -0.61 and r = -0.81, respectively; dilated cardiomyopathy r = -0.79 and r = -0.66, respectively). At any given level of volume at onset of atrial systole and tension at end of atrial systole, however, active emptying fraction was lower in patients with dilated cardiomyopathy compared with those with aortic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Stenosis↗

Benefit of pacing and beta-blockers in idiopathic repetitive polymorphic ventricular tachycardia.

An 18-year-old woman presented with recurrent exercise-induced syncopal episodes and severe systolic dysfunction. ECG monitoring disclosed repetitive polymorphic ventricular complexes, paroxysms of bidirectional ventricular tachycardia, and nonsustained bursts of slow polymorphic ventricular tachycardia that increased in length and rate during exercise. Ventricular arrhythmias were refractory to medical treatment, which included verapamil and beta-blockers. Addition of permanent atrial pacing to beta-blocker therapy suppressed the arrhythmias and reversed systolic impairment in the following months.

Adolescent↗

Prosthesis-patient mismatch after aortic valve replacement predominantly affects patients with preexisting left ventricular dysfunction: effect on survival, freedom from heart failure, and left ventricular mass regression.

OBJECTIVE: The effect of prosthesis-patient mismatch on clinical outcome and left ventricular mass regression after aortic valve replacement remains controversial. Data on whether the clinical effect of prosthesis-patient mismatch depends on left ventricular function at the time of aortic valve replacement are lacking. This study examined the long-term clinical and echocardiographic effects of prosthesis-patient mismatch in patients with and without left ventricular systolic dysfunction at the time of aortic valve replacement. METHODS: Preoperative and serial postoperative echocardiograms were performed in 805 adults who underwent aortic valve replacement between 1990 and 2003 and who were subsequently followed up in a dedicated valve clinic (follow-up, mean +/- SD, 5.5 +/- 3.5 years; maximum, 14.2 years). Preoperative left ventricular function was defined as normal (ejection fraction > or =50%) in 548 patients and impaired (ejection fraction <50%) in 257 patients. RESULTS: Patients with impaired preoperative left ventricular function and prosthesis-patient mismatch (indexed effective orifice area < or =0.85 cm2/m2) had a decreased overall late survival (hazard ratio, 2.8; P = .03), decreased freedom from heart failure symptoms or heart failure death (odds ratio of 5.1 at 3 years after aortic valve replacement; P = .009), and diminished left ventricular mass regression compared with patients with impaired preoperative left ventricular function and no prosthesis-patient mismatch. These effects of prosthesis-patient mismatch were not observed in patients with normal preoperative left ventricular function. CONCLUSIONS: Prosthesis-patient mismatch at an indexed effective orifice area of 0.85 cm2/m2 or less after aortic valve replacement primarily affects patients with impaired preoperative left ventricular function and results in decreased survival, lower freedom from heart failure, and incomplete left ventricular mass regression. Patients with impaired left ventricular function represent a critical population in whom prosthesis-patient mismatch should be avoided at the time of aortic valve replacement.

Aged↗

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location.

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.

Cardiac Volume↗

Timing of operation for chronic aortic regurgitation.

Left ventricular systolic function is an important determinant of long-term prognosis in patients with chronic aortic regurgitation. Data from several centers, using invasive and noninvasive assessment of left ventricular function, indicate that long-term postoperative survival is excellent, even in symptomatic patients, if preoperative left ventricular systolic function is normal. The long-term postoperative results are significantly worse in symptomatic patients with preoperative left ventricular systolic dysfunction, many of whom appear to have irreversible left ventricular failure before the onset of symptoms and are at a risk of late postoperative death from congestive heart failure. However, within this high risk subgroup long-term prognosis is excellent for patients, despite left ventricular dysfunction, if preoperative exercise capacity is preserved. In these patients, left ventricular dysfunction is likely to be reversible after operation. Hence, all patients with left ventricular dysfunction at rest should undergo aortic valve replacement, even if severe symptoms and deterioration in exercise tolerance have not developed. Once exercise tolerance becomes limited in such patients, the likelihood of irreversible left ventricular dysfunction is increased, and long-term postoperative survival is threatened.

Aortic Valve↗

Impaired coronary flow reserve in NIDDM: a possible role for diabetic cardiopathy in humans.

Diabetic cardiopathy represents a cardiac disorder with involvement of myocardial, interstitial, coronary, and neural structures. One of the main manifestations refers to coronary microangiopathy, which has not yet been clearly identified. Coronary hemodynamics, including the determination of coronary flow reserve, were therefore analyzed in normal subjects and in nine patients with NIDDM and clinically suspected coronary heart disease but normal coronary arteriogram. Coronary flow reserve was determined as the quotient of baseline and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.). Coronary blood flow was measured quantitatively by the argon method. Systolic left ventricular function was analyzed by ventriculography and diastolic function by M-mode and Doppler echocardiography. Twelve healthy normotensive subjects served as the control group (CON). In the diabetic patients, maximal coronary flow was significantly reduced (172 +/- 50 vs. 395 +/- 103 ml/min x 100 g; P < 0.001), and minimal coronary resistance was increased (0.60 +/- 0.19 vs. 0.24 +/- 0.06 mmHg x min x 100 g/ml; P < 0.001). Coronary reserve in the diabetic subjects was markedly reduced (1.84 +/- 0.39 vs. 4.23 +/- 0.52; P < 0.001). No difference existed with respect to myocardial oxygen consumption (12.4 +/- 2.3 vs. 11.8 +/- 2.8 ml O2/100 g x min; NS). Global systolic function was normal in all patients (ejection fraction: NIDDM 72 +/- 13 vs. CON 77 +/- 12%, NS; CI: NIDDM 3.2 +/- 0.8 vs. CON 3.3 +/- 1.2 l/min x m2, NS). Diastolic function was impaired in diabetic patients with an increase in relaxation time index (97 +/- 23 vs. 45 +/- 18 ms; P < 0.01) and an impaired diastolic inflow pattern, indicated by the ratio between early and late transmitral flow (0.75 +/- 0.14 vs. 1.66 +/- 0.13; P < 0.05). We conclude that the markedly reduced coronary flow reserve in diabetic patients may play a key role in the induction and perpetuation of coronary insufficiency in myocardial ischemia, in diastolic and systolic dysfunction, and in the initiation of diabetic cardiopathy.

Aged↗

Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy.

Epidemiologic studies have shown an important increase in the high mortality of patients with congestive heart failure (CHF) despite optimal medical management. Ventricular arrhythmia was recognized as the most common cause of death in this population. Electrolyte imbalance, myocardial fibrosis, left ventricular dysfunction, and inappropriate neurohumoral activation are presumed responsible for sudden cardiac death. In this study, we focused on the deleterious effects of the overproduction of aldosterone that occurs in patients with CHF. Secondary hyperaldersteronism can be part of several factors thought to be responsible for sudden cardiac death. We randomized 35 patients (32 men, aged 48 +/- 9 years) with systolic dysfunction (ejection fraction 33 +/- 5%) and New York Heart Association class III CHF secondary to dilated or ischemic cardiomyopathy into 2 groups. The treatment group received spironolactone, an aldosterone receptor antagonist, along with standard medical management using furosemide, angiotensin-converting enzyme inhibitors, and digoxin. The control group received only the standard medical treatment. Holter monitoring was used to assess the severity of ventricular arrhythmia. After 20 weeks, patients who received spironolactone had a reduced hourly frequency of ventricular premature complexes (VPCs) (65 +/- 18 VPCs/hour at week 0 and 17 +/- 9 VPCs/hour at week 16) and episodes of nonsustained ventricular tachycardia (VT) (3.0 +/- 0.8 episodes of VT/24-hour period at week 0, and 0.6 +/- 0.3 VT/24-hour period at week 16). During monitored treadmill exercise, a significant improvement in ventricular arrhythmia was found in the group receiving spironolactone (39 +/- 10 VPCs at week 0, and 6 +/- 2 VPCs at week 16). These findings suggest that aldosterone may contribute to the incidence of ventricular arrhythmia in patients with CHF, and spironolactone helps reduce this complication.

Analysis of Variance↗

Presentation and echocardiographic markers of neonatal hypertensive cardiomyopathy.

BACKGROUND: Systemic hypertension is a rare but important cause of neonatal heart failure. It is critical that this etiology be recognized and distinguished from other causes of myocardial dysfunction in young infants, because diagnostic studies, treatments, and prognoses are quite different. METHODS: Between 1991 and 2005, 11 neonates were diagnosed as having neonatal cardiomyopathy and systemic hypertension through retrospective review of the Children's Hospital of Wisconsin database. RESULTS: All infants in the cohort were found to have systemic hypertension (blood pressure of > 95th percentile for gestational age and weight). Causes included renovascular disease (n = 9), aortic obstruction secondary to thrombus (n = 1), and steroid use (n = 1). Echocardiography was performed at presentation for all patients because of cardiomegaly and/or hypertension. Echocardiographic findings were consistently striking for (1) left ventricular systolic dysfunction without chamber dilation, (2) concentric left ventricular hypertrophy, (3) left atrial dilation, and (4) aortomegaly. No anatomic aortic arch obstruction was identified, but Doppler findings for the descending thoracic aorta were uniformly consistent with elevated systemic vascular resistance. One patient died as a result of overwhelming thrombotic disease; all other patients responded to afterload reduction therapy with normalization of left ventricular systolic function during infancy. CONCLUSIONS: Hypertensive cardiomyopathy can present in neonates with nonspecific symptoms and systemic hypertension. Because sometimes hypertension in infants is ignored or misinterpreted as agitation, echocardiography can provide critical markers of the disease.

Aorta↗

An integrated approach to diagnosis and therapeutic management of patients with systolic heart failure in the Copenhagen metropolitan area.

BACKGROUND: Studies on the effect of heart failure clinics have been encouraging and convincing with respect to reduced hospitalizations, improved quality of life, and reduced cost. However, previous results have been derived from patient populations either recently discharged and with specific exclusion criteria or from heart transplant lists. We here report the establishment of a heart failure clinic that offers an integrated approach to both diagnosing and managing heart failure patients, the baseline characteristics of the first 283 patients treated, and the impact on heart failure hospitalizations during establishment. METHODS: Since September l, 1999, a heart failure clinic has been in operation at Frederiksberg University Hospital. The clinic was designed with both a diagnostic and a therapeutic unit. The diagnostic unit offers open access to all patients with suspected heart failure, either through referral from general practitioners or from the medical departments of the hospital. In the case of confirmed systolic heart failure, the patient is referred to the therapeutic unit for (1) uptitration and optimization of medical therapy and thorough information and education. In addition, the unit offers a rapid access track and the possibility of intravenous diuretic treatment. RESULTS: During the 21 months of operation, a total of 460 patients were referred to the clinic. Of these, 320 (70%) were found to have clinical evidence of heart failure, and 283 (88% of the patients with heart failure) had left ventricular systolic dysfunction (defined by an ejection fraction of < or =45%). These patients were seen in the clinic for education, control of fluid retention, and uptitration of medications. These patients with left ventricular dysfunction were predominantly elderly (aged 72.7 +/- 10.7 y) and most often male (73%). Ischemic heart disease was the most common etiology (55%). Before referral, most patients with left ventricular dysfunction had been treated with none or only low-dose angiotensin-converting enzyme inhibitor (55%), and fewer than one third received beta-blockers (29%). During the first year of operation of the clinic, there was a 23% decline of heart failure-related hospital admissions to the department of cardiology (from 396 to 306). CONCLUSIONS: Patients with systolic heart failure are not always optimally treated. The establishment of a heart failure clinic, which offers the combination of diagnosing and managing congestive heart failure, appears to be efficient both in terms of therapy optimization and with respect to a concomitant decline in hospitalization for heart failure.

Adolescent↗

Clinical syndrome suggestive of heart failure is frequently attributable to non-cardiac disorders--population-based study.

AIM: To assess how often the clinical syndrome (CS) of heart failure is attributable to alternative, including non-cardiac, explanations. METHODS AND RESULTS: Cross-sectional evaluation of 739 community participants aged>or=45 years. Subjects with >or=2 symptoms or signs (dyspnoea or fatigue, orthopnoea, nocturnal paroxysmal dyspnoea, third heart sound, jugular venous distension, rales and lower limb oedema) or who were receiving loop diuretics were considered to have the clinical syndrome of heart failure. Attributable fractions were derived based on adjusted odds ratios and the prevalence of underlying disorders among cases. CS was present in 28.0% of women and in 15.2% of men, p<0.001. The multivariate-adjusted fraction of CS attributable to female gender was 40.6%, to age>or=65 years 28.5%, left ventricular systolic dysfunction, left ventricular dilatation or moderate-severe valvular disease 4.9%, diastolic dysfunction or atrial fibrillation 13.0%, obesity 22.6%, coronary heart disease 7.2% and chronic lung disease 6.9%. When additionally adjusting for depressive symptoms, the association with gender and age became much weaker, and 32% of cases were attributable to depressive symptoms. Forty-two percent of subjects with CS had cardiac abnormalities. CONCLUSION: In less than half of subjects with CS was systolic or diastolic heart failure confirmed. Female gender, older age, obesity and depressive symptoms accounted for the largest fraction of CS.

Age Factors↗

Echo doppler assessment of left ventricular function in rats with hypertensive hypertrophy.

OBJECTIVE: This study attempted to establish echocardiographic measurements of left ventricular (LV) mass and LV systolic and diastolic function, particularly in rats with hypertensive heart. METHODS: M-mode LV echograms and Doppler mitral flow were obtained in Dahl salt-sensitive rats placed on 0.3% or 8% sodium chloride diet. Echo Doppler measurements were compared with catheterization and pathologic measurements in 54 rats for LV mass and in 45 rats for LV systolic and diastolic function. RESULTS: Echocardiographic measurement of LV mass correlated well with pathologic measurement (r = 0.94, P <.01, n = 54, SEE = 0.08 mg), independent of LV size, aging, and therapeutic intervention. Endocardial fractional shortening (FS) correlated with LV peak + dP/dt (r = 0.56, n = 45, P <.01), and the correlation was improved to r = 0.71 if 11 rats with marked LV hypertrophy were excluded. Midwall FS correlated well with LV peak + dP/dt (r = 0.72, n = 45, P <.01) even if rats with extremely thickened ventricular wall were included. If midwall FS was lower than 14%, LV systolic dysfunction was very likely (sensitivity 67%, specificity 91%). Association of mitral E/A ratio of 2.0 or greater with deceleration time of shorter than 35 ms was an accurate indicator of elevated LV end-diastolic pressure (sensitivity 82%, specificity 86%) and increased lung weight because of congestive heart failure (sensitivity 89%, specificity 96%) in rats with hypertension. CONCLUSION: LV mass, LV systolic function, and LV end-diastolic pressure were assessable with echo Doppler in rats with hypertensive heart.

Animals↗

Early detection of cardiac dysfunction in patients with anorexia nervosa by tissue Doppler imaging.

BACKGROUND: Cardiac damage is a major complication of chronic starvation. The aim of this study was to evaluate the changes of left ventricular function in patients with anorexia nervosa by means of pulsed tissue Doppler imaging. METHODS: A total of 20 females (age 22.4+/-4.3 years) with overt anorexia nervosa, 20 matched healthy thin females with body mass index < 19 kg/m2 and 20 matched healthy normal-weight females underwent both standard echocardiography and tissue Doppler imaging. Myocardial systolic wave (Sm) and early (Em) and atrial (Am) diastolic waves were measured on the basal lateral segment and the basal interventricular septum from the apical four-chamber view. RESULTS: When compared with control groups, the anorexia nervosa group showed lower left ventricular mass (p < 0.0001), lower Sm peak of both lateral wall (6.5+/-0.9 vs. 9.4+/-2.1 and vs. 9.5+/-1.9 cm/sec, p < 0.001) and septum (5.6+/-1.5 vs. 8.6+/-1.6 and vs. 8.8+/-1.5 cm/sec, p < 0.001), and comparable Em, Am and Em/Am ratio. The ratio between transmitral peak E and Em was significantly greater in anorexic patients than in controls (lateral wall: 8.1+/-0.1 vs. 6.8+/-0.2 and vs. 6.9+/-0.2, p < 0.001; septum: 10.8+/-0.4 vs. 8.8+/-0.5 and vs. 8.8+/-0.3, p < 0.001). No differences were observed between thin and normal-weight females. In the anorexia nervosa group, S(m) peak was significantly related to left ventricular mass indexed, at both septum (r = 0.55, p < 0.02) and lateral wall (r = 0.49, p < 0.03) levels. CONCLUSIONS: These results show that anorexia nervosa is associated with left ventricular systolic dysfunction, which is related with the reduction of cardiac mass. Tissue Doppler imaging can give useful information in the identification of regional left ventricular dysfunction, in addition to traditional parameters.

Adult↗

Effects of nitroprusside on cardiac norepinephrine spillover and isovolumic left ventricular relaxation in the normal and failing human left ventricle.

BACKGROUND: Left ventricular isovolumic relaxation responses to changes in afterload or preload may be mediated, in part, by reflex changes in sympathetic nervous system activity. PATIENTS AND METHODS: The authors examined whether changes in left ventricular isovolumic relaxation during changes in load were associated with changes in cardiac norepinephrine spillover. Six patients with normal left ventricular function and 12 patients with congestive heart failure secondary to left ventricular systolic dysfunction were studied. Measurements of left ventricular isovolumic relaxation (Tau) were obtained using a high fidelity left ventricular pressure manometer, before, during and after infusion of nitroprusside. Total body and cardiac norepinephrine spillover were measured using a radiotracer infusion. RESULTS: Nitroprusside caused significant reductions in systemic arterial and left ventricular end-diastolic pressures, changes that were similar in the two groups. In people with normal left ventricular systolic function, these changes were associated with significant increases in both systemic and cardiac sympathetic activity, but no change in Tau. In the group with congestive heart failure, cardiac norepinephrine spillover did not change; however, there was a significant increase in the rate of left ventricular isovolumic relaxation. CONCLUSION: This study confirms that in the failing human left ventricular, isovolumetric relaxation is sensitive to changes in loading conditions induced by the nitrosovasodilator nitroprusside. Importantly, this load sensitivity is not associated with reflex increases in cardiac sympathetic activity.

Cardiac Catheterization↗

Importance of wall motion analysis in the diagnosis of left main disease using stress nuclear myocardial perfusion imaging.

We describe a case of a 54-year-old male who underwent exercise technetium-99m sestamibi myocardial perfusion imaging prior to his renal transplantation. With exercise, the patient's myocardial perfusion imaging did not show any transient or fixed myocardial perfusion abnormalities due to balanced ischemia. However, wall motion analysis showed a new global left ventricular systolic dysfunction on post-exercise images. Coronary angiography showed severe left main coronary lesion involving ostia of left anterior descending, ramus intermedius and left circumflex coronary arteries with moderate right coronary artery disease. If one had used the perfusion imaging alone in this patient, the severe multivessel disease including left main coronary disease could have been missed. In this article we emphasize the importance of wall motion analysis in patients undergoing myocardial perfusion imaging.

Blood Pressure↗