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PubMed2003

Progression from compensated hypertrophy to failure in the pressure-overloaded human heart: structural deterioration and compensatory mechanisms.

BACKGROUND: The progression of compensated hypertrophy to heart failure (HF) is still debated. We investigated patients with isolated valvular aortic stenosis and differing degrees of left ventricular (LV) systolic dysfunction to test the hypothesis that structural remodeling, as well as cell death, contributes to the transition to HF. METHODS AND RESULTS: Structural alterations were studied in LV myectomies from 3 groups of patients (group 1: ejection fraction [EF] >50%, n=12; group 2: EF 30% to 50%, n=12; group 3: EF <30%, n=10) undergoing aortic valve replacement. Control patients were patients with mitral valve stenosis but normal LV (n=6). Myocyte hypertrophy was accompanied by increased nuclear DNA and Sc-35 (splicing factor) content. ACE and TGF-beta1 were upregulated correlating with fibrosis, which increased 2.3-, 2.2-, and 3.2-fold over control in the 3 groups. Myocyte degeneration increased 10, 22, and 32 times over control. A significant correlation exists between EF and myocyte degeneration or fibrosis. Ubiquitin-related autophagic cell death was 0.5 per thousand in control and group 1, 1.05 in group 2, and 6.05 per thousand in group 3. Death by oncosis was 0 per thousand in control, 3 per thousand in group 1, and increased to 5 per thousand (groups 2 and 3). Apoptosis was not detectable in control and group 3, but it was present at 0.02 per thousand in group 1 and 0.01 per thousand in group 2. Cardiomyocyte mitosis was never observed. CONCLUSIONS: These structure-function correlations confirm the hypothesis that transition to HF occurs by fibrosis and myocyte degeneration partially compensated by hypertrophy involving DNA synthesis and transcription. Cell loss, mainly by autophagy and oncosis, contributes significantly to the progression of LV systolic dysfunction.

Aged↗
PubMed2002

Is there a long-term predictive value of intraoperative low-dose dobutamine echocardiography in patients who have coronary artery bypass graft surgery with cardiopulmonary bypass?

UNLABELLED: In patients with coronary artery disease, chronic regional left ventricular systolic dysfunction at rest may be caused by hibernating or by infarcted myocardium. Intraoperative low-dose dobutamine (LDD) echocardiography reliably predicts the immediate recovery of regional myocardial function after coronary artery bypass graft (CABG) surgery. We sought to determine whether intraoperative LDD echocardiography would also predict recovery of regional function after 1 yr. Twenty-five patients with coronary artery disease who underwent CABG surgery with intraoperative LDD echocardiography were evaluated 1 yr later with a follow-up transthoracic echocardiogram. The covariates of left ventricular ejection fraction, old myocardial infarction, and diabetes mellitus were considered in an analysis of regional wall motion (RWM). A 16-segment model and a 1-5-point scoring system were used to evaluate 350 myocardial segments. Multiple logistic regression analysis was performed to determine whether response to intraoperative LDD echocardiography (5 microg. kg(-1). min(-1)) predicted changes in regional function at 1 yr. A segment was defined as stunned if the RWM score obtained during LDD infusion deteriorated after cardiopulmonary bypass but recovered in the 1-yr follow-up echocardiogram. A response to intraoperative LDD predicted changes in regional function at 1 yr. The overall odds of improvement in regional function were 2.22 times greater (95% confidence interval = 1.29, 3.82; P = 0.0039) with a positive response to intraoperative LDD. The positive predictive value of intraoperative LDD echocardiography for improvement in myocardial function was 0.81 and the negative predictive value was 0.34. The predictive values did not vary with the examined covariates. Of segments with unexpected deterioration of RWM immediately after cardiopulmonary bypass, 87% recovered at the time of the 1-yr follow-up echocardiogram. Contractile reserve demonstrated by intraoperative LDD echocardiography predicts regional function at 1 yr; however, the test cannot predict which segment will not recover. Most of unexpected regional ventricular systolic dysfunction immediately after CABG surgery can be attributed to myocardial stunning. IMPLICATIONS: In patients undergoing coronary artery bypass graft surgery, intraoperative low-dose dobutamine echocardiography has only limited value for the prediction of regional myocardial function at 1 yr. Small-dose dobutamine echocardiography predicts regional myocardial function at 1 yr when baseline regional wall motion abnormalities improve with dobutamine; however, the test cannot be used to predict which segment will not recover at 1 yr.

Adrenergic beta-Agonists↗
PubMed1993

Left ventricular diastolic impairment in type 1 diabetic patients with microalbuminuria.

The high incidence of cardiac mortality in type 1 diabetic patients is further increased when diabetic nephropathy is present. Since microalbuminuria (albumin excretion rate > 30 mg/day) represents an incipient stage of diabetic nephropathy, we decided to investigate whether incipient renal changes correlate with early diastolic cardiac dysfunction, known to preceed systolic dysfunction. To test this hypothesis, 13 normotensive type 1 diabetics with incipient nephropathy (mean age 37.8 +/- 3.5, diabetes duration 18.8 +/- 2.6 years), 13 type 1 diabetics without nephropathy (matched for age, diabetes duration and metabolic control) or other microangiopathic changes and 13 normal controls were studied. Diseases known to affect left ventricular performance were ruled out before investigation. Right and left ventricular parameters were assessed by M-mode and Doppler echocardiography. While parameters for left ventricular systolic function stayed within the normal range and did not differ between the two diabetic groups (ejection fraction 69.3 +/- 2.4 vs. 69.6 +/- 1.4%; fractional shortening 40.3 +/- 2.2 vs. 38.5 +/- 1.1%), diastolic function was significantly impaired in diabetic patients with microalbuminuria. This is expressed by an inversed early and late peak flow velocity ratio in patients with microalbuminuria (0.988 +/- 0.04 vs. 1.362 +/- 0.1; p < 0.05) and a significant percentual increase in late (atrial) filling (39.1 +/- 1.7 vs. 29.9 +/- 1.4% when compared to whole filling; p < 0.05) despite a similar rate-corrected isovolumetric relaxation period in both diabetic groups (98.4 +/- 5.8 vs. 95.5 +/- 6.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Determinants of left ventricular systolic function recovery after an acute coronary syndrome.

INTRODUCTION: Ischemic heart disease is a major cause of heart failure in western societies. However, the factors that may influence left ventricular function (LVF) recovery after an acute coronary syndrome (ACS) are still unclear. OBJECTIVE: To identify variables that may influence LVF evolution one year after ACS. METHODS: 104 patients hospitalized with ACS between 7/1/2001 and 12/31/2002 and with systolic dysfunction--defined as an echocardiographic ejection fraction (EF) < or = 45%--were randomly allocated to a planned coronary follow-up program (FUP) or a general cardiology clinic (GC); patients from both groups were also randomly referred to a structured cardiac rehabilitation program (CRP). EF was re-assessed at one year. We compared differences between patients who recovered left ventricular function (EF > 45%; group 1) and those who did not (group 2). RESULTS: One year after discharge, 44.2% of the patients had recovered function. There were no significant differences between the groups in gender (77.7 vs. 76.5% male), age (56 vs. 59 years), hypertension, diabetes, dyslipidemia, smoking habits or family history. A previous history of cardiovascular events was more frequent in group 2 (11.1% vs. 35.3%, p = 0.03). Cardiac catheterization was performed before discharge in 88.8% and 88.2% in groups 1 and 2 respectively (p = NS); no differences were found in coronary anatomy between the two groups. Angioplasty was performed in 54.2% in group 1 and 50% in group 2 (p = NS). There were no differences in the use of angiotensin-converting enzyme inhibitors (83.3% vs. 87.5%), beta-blockers (87.5% vs. 87.5%), nitrates (37.5% vs. 33.3%), aspirin (95.8% vs. 95.8%), statins (79.1% vs. 75%) or diuretics (20.8% vs. 45.8%). There was no significant difference in LVF recovery between patients randomized to FUP or GC (38.5% vs. 54.5%). 87.5% of patients who completed the CRP had normal EF at one year compared to 32.7% of patients not referred to the program (p = 0.009). Although EF improved in both groups, this improvement was greater in patients who completed a CRP (EF 8% vs. 5%, p = 0.003). CONCLUSION: A previous cardiovascular event and completion of a CRP were the only variables that influenced LVF recovery. Thus, enrollment in a CRP, in addition to standard therapy, could be an important therapeutic measure in patients with systolic dysfunction after ACS; our data suggest that these programs should be more widely used.

Aged↗
PubMed2005

Functional assessment by myocardial performance index (Tei index) correlates with plasma brain natriuretic peptide concentration in patients with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) might exhibit not only diastolic, but also latent systolic dysfunction. Therefore combined assessment of both systolic and diastolic function using myocardial performance index (Tei index) can be useful in HCM. Plasma brain natriuretic peptide (BNP) level is reported to be elevated in HCM, but the mechanism of BNP elevation in HCM remains to be established. METHODS AND RESULTS: The value of Tei index in 45 HCM patients was compared with that of 20 normal control subjects. The HCM patients showed a higher value of Tei index (0.55+/-0.12 vs 0.36+/-0.08, p < 0.0001) and longer isovolumic relaxation and contraction times than control subjects. The plasma BNP level correlated with Tei index in non-obstructive HCM (n = 35, r = 0.61, p < 0.0001), although the correlation was mild when overall HCM patients were included (r = 0.34, p = 0.02). The correlation was still significant after adjusting for age, or the extent and severity of left ventricular hypertrophy. Multiple stepwise regression analysis identified mitral E/A ratio (r = 0.49, F = 13.1) and Tei index (r = 0.37, F = 7.6) as independent predictors of higher plasma BNP level in non-obstructive HCM. CONCLUSIONS: Myocardial performance index was abnormal in HCM, reflecting both systolic and diastolic dysfunction in this disorder. Plasma BNP level correlated with functional assessment by Tei index in non-obstructive HCM.

Adult↗
PubMed2001

Digitalis for treatment of congestive heart failure in patients in sinus rhythm.

BACKGROUND: Digitalis glycosides have been in clinical use in the treatment of congestive heart failure for more than 200 years. In recent years several trials have been conducted to address concerns about efficacy and toxicity. Although a systematic review of the literature was recently published, an update is required to include more current trials. OBJECTIVES: To examine the effectiveness of digitalis glycosides in treating congestive heart failure in patients with normal sinus rhythm. To examine the effect of digitalis in patients taking diuretics, ACE inhibitors, and beta blockers; patients with varying severity and duration of disease; patients with prior exposure to digitalis vs. no prior exposure; and patients with diastolic vs. systolic dysfunction. SEARCH STRATEGY: Electronic databases were searched between 1966 and 2000. Dissertation Abstracts and annual meeting abstracts of the American Heart Association, American College of Cardiology, and European Society of Cardiology were searched from 1996-2000. In addition, reference lists provided by the pharmaceutical industry (Glaxo Wellcome Inc.) were searched. SELECTION CRITERIA: Included were randomized placebo-controlled trials of 20 or more adult patients of either sex with symptomatic congestive heart failure who were studied for seven weeks or more. Excluded were trials in which the prevalence of atrial fibrillation was 2% or greater, or in which any arrhythmia that might compromise cardiac function or any potentially reversible cause of heart failure such as acute ischemic heart disease or myocarditis was present. DATA COLLECTION AND ANALYSIS: Articles selected from the searches described above were reviewed by one of the coauthors, and validated by staff from the central office of the Heart Collaborative Review Group in Bristol, UK. MAIN RESULTS: Eleven articles meeting the defined criteria were identified, and major endpoints of mortality, hospitalization, and clinical status, based respectively upon on 8, 4, and 10 of these selected studies, were recorded and analyzed. The data show that there is no difference in mortality between treatment and control groups, whereas digitalis therapy is associated with a lower rate of hospitalization and of clinical deterioration. REVIEWER'S CONCLUSIONS: The literature indicates that digitalis has a useful role in the treatment of patients with congestive heart failure who are in normal sinus rhythm.

Cardiotonic Agents↗
PubMed2003

[Left ventricular systolic and diastolic dysfunction in patients with chronic renal failure treated with hemodialysis].

Systolic and diastolic left ventricular dysfunction is common and important predictor of risk of death in end-stage renal failure. Systolic dysfunction is defined echocardiographically by a shortening fraction < 25% or an ejection fraction < 40%. Systolic dysfunction has a poor prognosis, strongly associated with myocardial ischemia and left ventricular hypertrophy (LVH). Diastolic dysfunction combines relaxation problems with compliance abnormalities and usually is associated with LVH. It is not clinically possible to distinguish systolic from diastolic LV dysfunction. This underlines the importance of echocardiographic diagnosis. In the present study we have analysed echocardiographically the left ventricular systolic and diastolic function and some possible risk factors contributing to its dysfunction development in patients with chronic renal failure (crf) treated by hemodialysis (HD). From a cohort of 85 patients with crf we selected for analysis 59 clinically stable patients. Echocardiography (ECHO), ECG, body mass index (BMI), serum creatinine, urea, total protein, albumin, hemoglobin, hematocrit, electrolytes, endothelin (ET-1) and parathyroid hormone (PTH) concentrations were evaluated in all patients after HD session. In all HD patients systolic and diastolic LV dysfunction was observed as well as LVH: concentric LVH was detected by ECHO in 46 patients and in 13 patients excentric LVH was observed. Mean serum concentrations of urea, creatinine, endothelin (ET-1), PTH and phosphate were increased while serum concentration of hemoglobin, total protein, albumin, sodium, potassium, calcium were in the normal range. Positive correlation was found between PTH serum concentration and LVM r = 0.704 (p < 0.001), between PTH serum concentration and IVS r = 0.267 (p < 0.04), between PTH serum concentration and PW r = -0.238 (p < 0.04), between ET-1 and RWT r = 0.447 (p < 0.04) and negative correlation between BMI and LVMI r = -0.451 (p < 0.05). Our observations suggests that uremic cardiomyopathy is heterogenous (systolic and diastolic dysfunction) and multifactoral. The correlations between serum PTH concentration and LVH and between BMI and LVH confirmed that both hyperparathyroidism and malnutrition are important factors influencing the development of LVH which plays an important role in the systolic and diastolic cardiac failure in HD patients.

Adult↗
PubMed1985

Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia.

Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2003

Diagnosis of coronary vasospasm by detection of postischemic regional left ventricular delayed relaxation using echocardiographic evaluation with color kinesis.

BACKGROUND: Coronary vasospasm has been diagnosed by invasive provocative procedures during coronary arteriography. It would be useful to have a reliable, noninvasive, and safe diagnostic method for coronary vasospasm. Regional left ventricular (LV) diastolic dysfunction may persist without systolic dysfunction after an episode of coronary vasospasm. Color kinesis (CK) has been recently developed to facilitate the echocardiographic evaluation of regional wall motion. HYPOTHESIS: Color kinesis may be useful for diagnosis of coronary vasospasm by detection of postischemic regional LV diastolic wall motion abnormality. METHODS: Fifty-one consecutive patients with the last chest symptom within 2 weeks (4 +/- 3 days) were studied echocardiographically. Regional fractional area change during the first 30% of LV filling time in percentage of the segmental end-diastolic area change (CK diastolic index) was used to identify diastolic endocardial motion asynchrony. RESULTS: After diagnostic coronary arteriography with spasm provocation, 26 patients were diagnosed with coronary spastic angina (CSA) and the other 25 with chest pain syndrome (CPS). Regional delayed relaxation (CK-diastolic index < or = 50%) or diastolic asynchrony had been observed in at least one region in 25 (96%) patients with CSA, whereas it had been noted in 2 (8%) patients with CPS. In 17 (65%) patients with CSA, it had been detected in multiple vascular territories, suggesting multivessel spasm. The diastolic asynchrony disappeared in CSA after a month of angina-free period. CONCLUSION: Analysis of CK images allows identification of regional LV delayed relaxation or diastolic asynchrony in patients with coronary vasospasm, differentiating them from patients with chest pain syndrome (sensitivity 96%, specificity 92%).

Acetylcholine↗
PubMed2005

[Thyroid and cardiovascular system].

The cardiocirculatory changes in hyperthyroidism seem to be an accommodation to the increased metabolic demands and lead to an increased perfusion of the peripheral tissues. Due to the influence of elevated thyroid hormone levels, contractility, stroke volume, resting heart rate, and contraction and relaxation velocity of the left ventricle increase. Caused by direct effect on the smooth vascular muscle, systemic vascular resistance is decreased with the consequence of a diminished afterload and an increased cardiac efficiency. The activation of the renin-angiotensin-aldosteron system and the increased production of erythropoietin additionally lead to an increased blood volume, which increases cardiac preload together with the increased venous backflow. Manifest hypothyroidism is characterized by bradycardia and diastolic dysfunction in rest and systolic dysfunction at stress. Despite a slight increase of diastolic blood pressure due to an increased systemic vascular resistance, blood pressure remains nearly stable because of diminished cardiac output. Hypercholesterinaemia and diastolic hypertension in hypothyroid patients can lead to the development of arteriosclerosis and coronary heart disease (CHD). Also subclinical hypothyroidism is associated with a significantly higher risk for arteriosclerosis and CHD, whereas subclinical hyperthyroidism seems to be associated with an increased mortality for all reasons, especially for cardiovascular diseases.

Cardiovascular System↗
PubMed1990

Right atrial compression in postoperative cardiac patients: detection by transesophageal echocardiography.

Four patients developed hypotension after heart surgery. Hemodynamic measurements revealed elevated right atrial pressure with normal pulmonary capillary wedge pressure. Conventional transthoracic two-dimensional echocardiography was technically suboptimal for detection of pericardial effusion. In each patient transesophageal echocardiography demonstrated significant compression of the right atrium by a localized mass. At reoperation atrial compression by an organized hematoma was found and in each instance successfully drained. Thus, transesophageal echocardiography is superior to transthoracic echocardiography in evaluating critically ill postoperative hypotensive patients and can differentiate isolated right atrial tamponade from other causes of hemodynamic deterioration such as prosthetic valve dysfunction or left ventricular systolic dysfunction, or both.

Aged↗
PubMed1995

Response of hypertensive left ventricular hypertrophy and coronary microvascular disease to calcium antagonists.

Hypertensive left ventricular hypertrophy comprises not only myocyte hypertrophy, but is often associated with interstitial fibrosis and structural alterations of the coronary microcirculation. The consequences are early diastolic dysfunction and often later systolic dysfunction of the left ventricle, resulting in congestive heart failure. Involvement of the coronary resistance vessels leads to an impairment of coronary flow reserve despite normal epicardial arteries. Therefore, antihypertensive treatment should aim at reversing myocyte hypertrophy, restoring myocardial structure, and improvement in coronary flow reserve apart from blood pressure lowering. Many clinical studies have shown that calcium antagonists are effective in lowering blood pressure and can induce regression of left ventricular hypertrophy. Moreover, experimental studies have shown a restoration of myocardial structure. Recent clinical studies have demonstrated a marked improvement of the impaired coronary vasodilator reserve in hypertensive patients after long-term treatment with calcium antagonists. In summary, calcium antagonists can be regarded as an antihypertensive treatment modality that is able to restore myocardial structure and to repair coronary microcirculation and therefore can be considered as causative treatment of hypertensive cardiac remodeling.

Antihypertensive Agents↗
PubMed2003

Effect of thyroid hormone supplementation on survival of euthyroid dogs with congestive heart failure due to systolic myocardial dysfunction: a double-blind, placebo-controlled trial.

Nineteen euthyroid dogs of 12 breeds with echocardiographic signs of dilated cardiomyopathy (DCM) and radiographic and clinical signs of congestive heart failure (CHF) were evaluated in a randomised, double-blind, and placebo-controlled study. The dogs received either thyroxine or placebo as an adjunct to digoxin, furosemide and propranolol. The group assignment of individual dogs and serum concentrations of thyroid hormones remained unknown to owners and investigators during the entire study period. Dogs were evaluated clinically and with electrocardiography (ECG), thoracic radiography, echocardiography and measurement of total thyroxine (tT4) and thyroid stimulating hormone (TSH) before beginning of the trial, and then one week, 2 months, 6 months and yearly after initial examination, and, when applicable, at the time of euthanasia. End-point of the study was euthanasia (n = 17) due to severe congestive heart failure or sudden death (n = 2). Survival times ranged from 17 to 1030 days (median 187 days) in the placebo group, and from 18 to 1000 days (median 73 days) in the treatment group. There was no statistically significant difference in survival times between the treatment group and the placebo group (p = 0.46). Post mortem and histopathologic examinations revealed the attenuated wavy fiber type of DCM in 11 dogs, and myocardial infarcts, arteriosclerosis and chronic valvular disease in one dog. In conclusion, there was a wide range in survival times of dogs treated with digoxin, furosemide and propranolol. Adding thyroid hormones to the treatment did not significantly influence survival.

Animals↗
PubMed2005

Novel markers for heart failure diagnosis and prognosis.

PURPOSE OF REVIEW: This paper reviews recent advances in heart failure biomarkers for identification of disease precursors, subclinical disease, and onset or progression of overt disease. RECENT FINDINGS: Heart failure biomarkers can be categorized empirically as neurohormonal mediators, markers of myocyte injury and remodeling, and indicators of systemic inflammation. Brain natriuretic peptide is the most widely studied, with a potentially important but evolving role for determining prognosis and as a surrogate endpoint in clinical trials. Strong evidence exists for use of brain natriuretic peptide in the diagnosis of acute heart failure and for improved clinical outcomes with a brain natriuretic peptide-guided approach to heart failure care. The use of brain natriuretic peptide as a screening tool for asymptomatic left ventricular systolic dysfunction, or to distinguish systolic from diastolic heart failure, is not supported by current data. Markers of myocyte injury, including troponins, heart-type fatty acid binding protein, and myosin light chain-1, may further improve heart failure prognostication in conjunction with plasma brain natriuretic peptide. Biomarkers of matrix remodeling and inflammation have emerged as potential preclinical indicators to identify individuals at risk of developing clinical heart failure. A role for cellular adhesion molecules may also emerge in identifying those at risk for cardiovascular thrombotic complications, such as stroke. SUMMARY: The spectrum of heart failure biomarkers and their potential clinical applications continues to grow. Ongoing research on multimarker strategies will likely identify biomarker combinations that are optimal at various stages during the evolution of heart failure, ranging from their use for screening, diagnosis, determining prognosis, and guiding management.

Biomarkers↗
PubMed1982

Left ventricular function in hospitalized geriatric patients.

Left ventricular ejection fraction was measured by gated wall motion in 62 patients, 75 years old or older, admitted to a Geriatric Acute Assessment Ward. From this group, 42 patients not taking digitalis or other cardioactive medication were selected for analysis. Thirty of them had clinically identifiable heart disease, whereas 12 did not. Resting left ventricular ejection fractions in the 12 patients without clinically identifiable heart disease averaged 0.60 +/- 0.09. None had an ejection fraction below 0.50. In the 30 patients with clinically identifiable heart disease, mean ejection fraction was 0.49 +/- 0.15 (range 0.17-0.84), P less than 0.01. In the patients with heart disease, reduction of ejection fraction was correlated with either cardiac enlargement or congestive heart failure. Neither age nor electrocardiographic abnormalities added to the strength of this correlation. Fifty-eight per cent of patients with congestive heart failure had ejection fractions greater than or equal to 0.40, suggesting that congestive heart failure in this age group is frequently related to diastolic left ventricular dysfunction unaccompanied by major systolic dysfunction. The prognosis of patients with congestive heart failure and ejection fractions above 0.35 was significantly better than of patients with congestive heart failure and ejection fractions below 0.35. From these data and other data available in the literature, it is proposed that the lower limit for ejection fraction be 0.50 for patients 75 years old or older. Congestive heart failure in patients 75 years old or older appears to be associated with relatively higher ejection fractions or even with ejection fractions within the normal range. In these patients, digitalis may not be indicated, and short term-prognosis is relatively favorable.

Aged↗
PubMed2000

Altered stoichiometry of FKBP12.6 versus ryanodine receptor as a cause of abnormal Ca(2+) leak through ryanodine receptor in heart failure.

BACKGROUND: In the pathogenesis of cardiac dysfunction in heart failure, a decrease in the activity of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase is believed to be a major determinant. Here, we report a novel mechanism of cardiac dysfunction revealed by assessing the functional interaction of FK506-binding protein (FKBP12.6) with the cardiac ryanodine receptor (RyR) in a canine model of pacing-induced heart failure. METHODS AND RESULTS: SR vesicles were isolated from left ventricular muscles (normal and heart failure). The stoichiometry of FKBP12.6 per RyR was significantly decreased in failing SR, as assessed by the ratio of the B(max) values for [(3)H]dihydro-FK506 to those for [(3)H]ryanodine binding. In normal SR, the molar ratio was 3.6 ( approximately 1 FKBP12.6 for each RyR monomer), whereas it was 1.6 in failing SR. In normal SR, FK506 caused a dose-dependent Ca(2+) leak that showed a close parallelism with the conformational change in RyR. In failing SR, a prominent Ca(2+) leak was observed even in the absence of FK506, and FK506 produced little or no further increase in Ca(2+) leak and only a slight conformational change in RyR. The level of protein expression of FKBP12.6 was indeed found to be significantly decreased in failing SR. CONCLUSIONS: An abnormal Ca(2+) leak through the RyR is present in heart failure, and this leak is presumably caused by a partial loss of RyR-bound FKBP12.6 and the resultant conformational change in RyR. This abnormal Ca(2+) leak might possibly cause Ca(2+) overload and consequent diastolic dysfunction, as well as systolic dysfunction.

Animals↗
PubMed2000

Surgical treatment of valvular heart disease in patients with acromegaly.

BACKGROUND AND AIM OF THE STUDY: Acromegaly is associated with heart disease in one-third of patients, and diastolic dysfunction may precede global systolic dysfunction. Patients with acromegalic heart disease may have valvular disease, but the role of surgery in such patients has not been established. The purpose of this study was to document the outcome of surgery in a series of these patients from one institution. METHODS: Among 951 patients with the diagnosis of acromegaly seen at our institution since 1972, 10 (eight men, two women) have undergone operation for valvular heart disease. Average patient age was 62.2 +/- 11.5 years; average body weight was 84 +/- 13 kg; average height was 178 +/- 12 cm. The mean duration of acromegaly was 15.2 +/- 12.7 years. At the time of heart surgery, seven patients had active disease, defined by elevation of growth hormone levels, while three had inactive disease. Treatment of pituitary adenomas before valvular surgery included surgical resection in three patients and external-beam radiation treatment in four. The preoperative ejection fraction was 42 +/- 19% (range: 20% to 66%). Valve lesions included aortic stenosis in four patients, aortic regurgitation in four, and mitral regurgitation in three (one patient had double valve disease). RESULTS: Valve replacement was performed in all patients with aortic disease (two bioprostheses, six mechanical), and three patients with mitral regurgitation had repair. Concomitant procedures performed in seven patients included coronary bypass (two), left ventricular aneurysmectomy (two), and ligation of the left atrial appendage, septal myectomy and defibrillator insertion (one each). Early complications included endocarditis, low cardiac output and arrhythmia in one patient each. There were no perioperative deaths. One patient underwent reoperation ten years later for a perivalvular leak. CONCLUSION: Valvular surgery can be performed safely in acromegalic patients, even those with active endocrinopathy.

Acromegaly↗