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PubMed1993

["Severe" congestive heart failure at a medical center].

UNLABELLED: Heart failure (HF) is a dynamic clinical syndrome depending on multiple hemodynamic and neurohormonal factors. This syndrome concerns not only left ventricular systolic dysfunction but also left ventricular diastolic dysfunction and right ventricular dysfunction. Clinical features and therapeutic approaches are different for each of them. NYHA class IV is just one of the various prognostic factors of heart failure; consequently, severe heart failure is not synonymous of NYHA class IV. OBJECTIVE: To study hospitalised patients with heart failure in NYHA class IV, in order to characterise the predominant dysfunction, and analyze evolution and mortality. DESIGN: A retrospective analysis of a prospective study. SETTING: Hundred and eight hospitalised patients (1985-89). Patients with chronic obstructive pulmonary disease and acute myocardial infarction were excluded. PATIENTS: Sixty nine patients: 29 female and 40 male, aged 18 to 81 years old (m = 59 +/- 15.5). METHODS: Patients were clinically examined and had chest radiographs, electrocardiogram and M + 2D mode echocardiogram. Three groups were identified: Group I-patients with predominant left ventricular systolic dysfunction; Group II-patients with predominant left ventricular diastolic dysfunction; Group III-patients with predominant right ventricular dysfunction. RESULTS: 41% of the patients had coronary artery disease; 44%, valvular heart disease; 11.8% dilated cardiomyopathy; 8.7% hypertrophic cardiomyopathy; 8.7% hypertensive cardiomyopathy. Fifty five percent of the patients were in group I and the major aetiology were coronary artery disease and valvular heart disease; 25% of the patients were in group II and the major aetiology were coronary artery disease and hypertrophic cardiomyopathy; 20% of the patients were in group III, all had valvular heart disease. The global mortality during the hospitalisation period was 15.9%, mostly group III (29%) and II (17%). CONCLUSIONS: Heart failure patients in NYHA class IV formed an heterogeneous group, requiring individualised therapeutic approaches. Left ventricular systolic dysfunction was the major pathophysiological mechanism, however, diastolic dysfunction and right ventricular dysfunction were frequent. Coronary artery disease presented as a frequent aetiology of heart failure, resulting in diastolic and/or systolic dysfunction. Valvular heart disease can be present as left ventricular systolic or diastolic dysfunction or as a right ventricular dysfunction, depending on the valvulopathy and the time of evolution. Echocardiography, in association with clinical features, has been very useful for each patient approach, allowing HF aetiology and pathophysiological mechanisms characterisation. The low mortality observed in this study was related certainly to the correction of precipitating factors, together with early etiologic diagnosis and pathophysiological characterisation, and adequate individualised treatment.

Adolescent↗

PubMed2005

Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database.

UNLABELLED: Approximately 50% of patients hospitalized for heart failure have preserved systolic function. These patients are more likely to be older, women, and hypertensive. Their duration of hospitalization is similar to that of heart failure patients with systolic dysfunction, but their in-hospital mortality risk is lower. This mortality risk is increased in the setting of renal insufficiency, and the two most important risk predictors are elevated blood urea nitrogen and systolic blood pressure < or = 125 mm Hg. Medical treatment strategies for patients with preserved systolic function are inconsistent and reflect the need for efficacious evidence-based treatment regimens. OBJECTIVES: The aims of this analysis were to describe the clinical characteristics, management, and outcomes of patients hospitalized for acute decompensated heart failure (HF) with preserved systolic function (PSF). BACKGROUND: Clinically meaningful characteristics of these patients have not been fully studied in a large database. METHODS: Data from >100,000 hospitalizations from the Acute Decompensated Heart Failure National Registry (ADHERE) database were analyzed. RESULTS: Heart failure with PSF was present in 50.4% of patients with in-hospital assessment of left ventricular function. When compared with patients with systolic dysfunction, patients with PSF were more likely to be older, women, and hypertensive and less likely to have had a prior myocardial infarction or be receiving an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker. In-hospital mortality was lower in patients with PSF compared with patients with systolic dysfunction (2.8% vs. 3.9%; adjusted odds ratio [OR]: 0.86; p = 0.005), but duration of intensive care unit stay and total hospital length of stay were similar. Serum creatinine >2 mg/dl was associated with increased in-hospital mortality in both systolic function groups (PSF: 4.8%; systolic dysfunction: 8.4%; p < 0.0001), and the most powerful predictors of in-hospital mortality in both groups were blood urea nitrogen >37 mg/dl (OR: 2.53; 95% confidence interval [CI]: 2.22 to 2.87) and systolic blood pressure < or =125 mm Hg (OR: 2.58; 95% CI: 2.33 to 2.86). CONCLUSIONS: Heart failure with PSF is common and is characterized by a unique patient profile. Event rates are worrisome and reflect a need for more effective management strategies.

Aged↗

PubMed1998

Systolic ventricular dysfunction causes selective diaphragm atrophy in rats.

In order to examine the relative impairment of the diaphragm and other skeletal muscles in systolic ventricular dysfunction (VD), their structure and function were compared between rats with VD induced by left coronary artery ligation (n = 17) and sham-operated rats (Co, n = 10). In addition, in an attempt to unravel the mechanism of the observed impairment, we examined alterations in insulin-like growth factor-I (IGF-I) serum levels and IGF-I expression in the liver, diaphragm, and gastrocnemius. In a second series of rats (VD, n = 5 and Co, n = 5) hemodynamic measurements were performed. All measurements were performed 3 mo after the operation. Infarct size averaged 32 +/- 10 and 44 +/- 20% in the two series, respectively (NS). Hemodynamic measurements revealed a decrease in left ventricular peak systolic pressure of 19% (p < 0. 05). Significant diaphragm atrophy (weight: 622 +/- 52 mg in VD versus 750 +/- 54 mg in Co, p < 0.0005), without alterations in diaphragm contractile properties was present in VD animals. For all animals combined, the reduction in diaphragm weight was related to infarct size (r = -0.74, p < 0.001). No alterations were observed in the other inspiratory and peripheral muscles. ATPase staining of the diaphragm showed atrophy of type I and type IIx/b fibers, their cross-sectional area (CSA) being reduced by 13 and 16%, respectively (p < 0.05). There were no signs of myopathic alterations. IGF-I expression was increased by 55% in the diaphragm of rats with VD (p < 0.05). IGF-I expression in the liver and gastrocnemius and serum IGF-I levels were unaltered. These data suggest the presence of compensatory mechanisms aimed at minimizing diaphragmatic fiber atrophy. We conclude that systolic VD caused: (1) selective diaphragm atrophy, which was related to infarct size; (2) a decrease in diaphragm type I and IIx/b CSA not associated with myopathic changes; (3) an increase in the IGF-I mRNA content of the diaphragm. The selective diaphragm involvement in the present study may be related to the moderate degree of ventricular dysfunction induced.

Adenosine Triphosphatases↗

PubMed2000

Safety and costs of initiating angiotensin converting enzyme inhibitors for heart failure in primary care: analysis of individual patient data from studies of left ventricular dysfunction.

OBJECTIVE: To estimate the costs and consequences of diagnosing symptomatic heart failure with left ventricular systolic dysfunction and initiating angiotensin converting enzyme inhibitors in primary care. DESIGN: Analysis of individual patient data from studies of left ventricular dysfunction (SOLVD) to identify complications during test dose and titration phases. SETTING: Two randomised controlled trials in secondary care. PARTICIPANTS: 7487 patients taking a test dose of enalapril at enrolment to the treatment and prevention trials; 2569 patients with clinical signs of heart failure and established left ventricular dysfunction entered the treatment trial. MAIN OUTCOME MEASURES: Discontinuation during the test dose period. Discontinuation or reduction of dose during the first year of treatment for heart failure. Costs of diagnosis and titration of treatment. RESULTS: During the test dose phase, 585 patients (7.8%) reported side effects; 136 (1.8%) of these discontinued because of severe side effects. During the titration phase, compared with placebo, enalapril was associated with an increased risk of dose reduction due to hypotension (odds ratio 2.09, 95% confidence interval 1.15 to 3.82). However, overall, there was no difference in the rates of side effects leading to dose reduction or withdrawal between the enalapril and placebo groups. The costs of diagnosing heart failure with left ventricular systolic dysfunction and initiating and titrating an angiotensin converting enzyme inhibitor in primary care are pound300 to pound400. CONCLUSIONS: Treatment with angiotensin converting enzyme inhibitors can be safely started for patients with heart failure and left ventricular systolic dysfunction in primary care.

Adult↗

PubMed1994

[Left ventricular insufficiency: systolic versus diastolic dysfunction].

Left ventricular failure has been subdivided into different forms. Systolic pump failure (= systolic dysfunction) and diastolic filling failure (= diastolic dysfunction) are important entities in the overall framework of heart failure. The clinical patterns of both are presented in light of 2 case reports: systolic dysfunction involves the combination of left ventricular failure, cardiomegaly and depressed systolic ejection fraction. Diastolic dysfunction is accompanied by pulmonary congestion in the presence of a normal or only slightly enlarged ventricle and a normal ejection fraction. Prognosis of systolic dysfunction is poor, with a 5-year survival rate of 40%, compared to 70% in patients with isolated diastolic dysfunction. Medical treatment of systolic dysfunction is based primarily on ACE-inhibitors followed by diuretics and digitalis. Betablockers in low doses and spironolactone can provide additional benefit. Calcium channel blockers are rarely indicated, due to their negative inotropic effects. In patients with diastolic dysfunction, however, they are the first choice because of their positive lusitropic effect on relaxation and ventricular filling. ACE-inhibitors are suitable in hypertensive heart disease, while diuretics and betablockers are second line drugs. Digitalis should be avoided since worsening of diastolic function may occur.

Cardiovascular Agents↗

PubMed2006

Association of parental heart failure with risk of heart failure in offspring.

BACKGROUND: The association between heart failure in parents and the prevalence of left ventricular systolic dysfunction and the risk of heart failure in their offspring has not been investigated in a community-based setting. METHODS: We examined the cross-sectional association of heart failure in parents with the prevalence of left ventricular systolic dysfunction, as well as left ventricular mass, internal dimensions, and wall thickness, in 1497 participants of the Framingham Offspring Study (mean age, 57 years; 819 women) who underwent routine echocardiography. We also investigated prospectively whether heart failure in parents increased the risk of heart failure in 2214 offspring (mean age, 44 years; 1150 women). RESULTS: As compared with the 1039 participants whose parents did not have heart failure, the 458 participants in the cross-sectional cohort who had at least one parent with heart failure were more likely to have increased left ventricular mass (17.0 percent vs. 26.9 percent), left ventricular internal dimensions (18.6 percent vs. 23.4 percent), and left ventricular systolic dysfunction (3.1 percent vs. 5.7 percent); the multivariable-adjusted odds ratios were 1.35 (95 percent confidence interval, 0.99 to 1.84), 1.29 (95 percent confidence interval, 0.96 to 1.72), and 2.37 (95 percent confidence interval, 1.22 to 4.61), respectively. In the longitudinal cohort, heart failure developed in 90 offspring during follow-up (mean length of follow-up, 20 years). The age- and sex-adjusted 10-year incidence rates of heart failure were 2.72 percent among offspring with a parent with heart failure, as compared with 1.62 percent among those without a parent with heart failure. This increase in risk persisted after multivariable adjustment (hazard ratio, 1.70; 95 percent confidence interval, 1.11 to 2.60). CONCLUSIONS: Heart failure in parents is associated with an increased prevalence of left ventricular systolic dysfunction cross-sectionally and an elevated risk of heart failure longitudinally. Our data emphasize the contribution of familial factors to the heart-failure burden in the community.

Adult Children↗

PubMed2001

[Cardiovascular ultrasound: applications for the assessment of cardiac function].

Congestive heart failure(CHF) is usually associated with impaired left ventricular(LV) systolic function, and thus, the measurement of systolic function is an essential component of the evaluation of any patients with known or suspected cardiac disease. Among many parameters, most frequently used are LV percent fractional shortening and ejection fraction(EF), which can be easily measured from an M-mode echocardiogram. However, these M-mode measurements may be inaccurate in patients with asymmetrical LV due to myocardial infarction, right ventricular overload or sigmoid septum. Especially in such cases, EF should be measured using two-dimensional echocardiography. Usually, LV volumes and EF are calculated using the disc-summation method through the manual tracing of apical two-chamber and four-chamber echocardiograms. On the other hand, it has been recognized that congestive heart failure may arise in the absence of any systolic dysfunction and CHF due to systolic dysfunction never occurs in the absence of concomitant diastolic dysfunction. Although the analysis of pulsed-Doppler transmitral flow velocity has been most widely used for the noninvasive assessment of LV diastolic function, an increase in left atrial pressure during CHF can pseudonormalize an abnormal flow pattern and mask LV diastolic dysfunction. Recently, we proposed a new index for assessing LV diastolic function, flow propagation velocity, which can be measured with color M-mode Doppler echocardiography and baseline-shift technique. Recent studies have shown that the flow propagation velocity is a unique noninvasive parameter of LV diastolic function which can accurately detect the diastolic impairment in patients with different types of cardiac diseases with various loading conditions.

Diastole↗

PubMed2006

Effects of nurse management on the quality of heart failure care in minority communities: a randomized trial.

BACKGROUND: Despite therapies proven effective for heart failure with systolic dysfunction, the condition continues to cause substantial hospitalization, disability, and death, especially among African- American and other nonwhite populations. OBJECTIVE: To compare the effects of a nurse-led intervention focused on specific management problems versus usual care among ethnically diverse patients with systolic dysfunction in ambulatory care practices. DESIGN: Randomized effectiveness trial conducted from September 2000 to September 2002. SETTING: The 4 hospitals in Harlem, New York. PATIENTS: 406 adults (45.8% were non-Hispanic black adults, 32.5% were Hispanic adults, 46.3% were women, and 36.7% were > or =65 years of age) who met eligibility criteria: systolic dysfunction, English- or Spanish-language speakers, community-dwelling patients, and ambulatory care practice patients. INTERVENTION: During a 12-month intervention, bilingual nurses counseled patients on diet, medication adherence, and self-management of symptoms through an initial visit and regularly scheduled follow-up telephone calls and facilitated evidence-based changes to medications in discussions with patients' clinicians. MEASUREMENTS: Hospitalizations (in 406 of 406 patients during follow-up) and self-reported functioning (in 286 of 406 patients during follow-up) at 12 months. RESULTS: At 12 months, nurse management patients had had fewer hospitalizations (143 hospitalizations vs. 180 hospitalizations; adjusted difference, -0.13 hospitalization/person-year [95% CI, -0.25 to -0.001 hospitalization/person-year]) than usual care patients. They also had better functioning: The Short Form-12 physical component score was 39.9 versus 36.3, respectively (difference, 3.6 [CI, 1.2 to 6.1]), and the Minnesota Living with Heart Failure Questionnaire score was 38.6 versus 47.3, respectively (difference, -8.8 [CI, -15.3 to -2.2]). Through 12 months, 22 deaths occurred in each group and percentages of patients who were hospitalized at least once were similar in each group (30.5% of nurse management patients vs. 36.5% of control patients; adjusted difference, -7.1 percentage points [CI, -16.9 to 2.6 percentage points]). LIMITATIONS: Three nurses at 4 hospitals delivered interventions in this modest-sized trial, and 75% of the participants were from 1 site. It is not clear which aspects of the complex intervention accounted for the results. CONCLUSIONS: Nurse management can improve functioning and modestly lower hospitalizations in ethnically diverse ambulatory care patients who have heart failure with systolic dysfunction. Sustaining improved functioning may require continuing nurse contact.

Adult↗

PubMed2005

[Heart failure and sudden death].

Sudden death in patients with heart failure (HF) is a topic of great complexity. Neurohumoral activation including adrenergic and renin-angiotensin-aldosterone system has been a suspected trigger for lethal ventricular arrhythmias and sudden deaths. Randomized clinical trials have demonstrated that angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists and beta-adrenergic blockers improve survivals in patients with HF. Although prophylactic implantable cardioverter defibrillator (ICD) therapy is effective reducing mortality in patients with left ventricular (LV) systolic dysfunction, the ICD is unlikely to be appropriate for all patients with LV systolic dysfunction. In addition, the effect of routine prophylactic use of ICDs on health care costs must be carefully considered. The care of patients with LV systolic dysfunction should be individualized for each patient.

Arrhythmias, Cardiac↗

PubMed1999

Differentiating systolic from diastolic heart failure using impedance cardiography.

OBJECTIVE: Differentiating systolic from diastolic congestive heart failure (CHF) is often difficult in the ED. Impedance cardiography (IC) allows for the noninvasive evaluation of systolic function and measurement of diastolic time intervals. This study was designed to assess the ability of IC to accurately measure isovolumic relaxation time (IVRT) and determine relative cardiac contractility, thereby differentiating systolic from diastolic mechanisms in acute CHF. METHODS: In an evaluation of the technique, the average differences in the diastolic time intervals measured in normal subjects by both IC tracings and phonocardiography were compared. Likewise, the average Heather index (HI) of patients with known systolic dysfunction (ejection fraction < 30% by echo-cardiography) was compared with the mean HI measured in the normal subjects. In a retrospective analysis, the clinical performance of the method was examined by extracting the values of IVRT and HI from IC tracings of patients presenting with CHF. The determined IVRT and HI values were then correlated to clinical markers for diastolic and systolic dysfunction. RESULTS: Analysis of 280 IC tracings in eight healthy volunteers revealed an average difference of 0.0075 seconds (95% CI = -0.0067 to 0.0217) when IVRT intervals measured by phonocardiography and IC are compared. The HI in this normal group averaged 14.2 (95% CI = 9.4 to 19.0), contrasting to the much lower value of 2.8 (95% CI = 1.98 to 3.62) seen in eight subjects with documented systolic dysfunction. In 26 patients with decompensated CHF, there was a close correlation (r = 0.81) of the measured IVRT to left ventricular hypertrophy by voltage criteria and while a fall in the HI was correlated with intravascular volume expansion. Though there was considerable overlap (46%) in mechanisms of CHF, 35% of the patients were found to have only systolic dysfunction (HI < 5 and IVRT < 0.125), while 19% had a predominantly diastolic etiology (IVRT > 0.125 and HI > 5) for their failure. CONCLUSION: IC measures of contractility and diastolic time intervals are a potentially effective method for differentiating the dominant mechanisms of CHF in the emergent setting and categorizing CHF patients into different subsets.

Acute Disease↗

PubMed2004

Furosemide and the progression of left ventricular dysfunction in experimental heart failure.

OBJECTIVES: We tested the hypothesis that furosemide accelerates the progression of left ventricular systolic dysfunction in a tachycardia-induced porcine model of heart failure. BACKGROUND: Furosemide activates the renin-angiotensin-aldosterone system in patients with congestive heart failure (CHF). Such activation may contribute to CHF progression, but prospective data are lacking. METHODS: Thirty-two Yorkshire pigs were randomized to furosemide (1 mg/kg intramuscularly daily, mean 16.1 +/- 0.9 mg) or placebo. Thereafter, a pacing model of heart failure was utilized to produce systolic dysfunction in both sets of animals (fractional shortening <0.16 by echocardiogram). The goal was to determine if furosemide would accelerate the progression of left ventricular dysfunction in the "treated" group. After sacrifice, sodium-calcium exchanger currents and their responsiveness to isoproterenol were measured during voltage clamp. All investigators were blinded to treatment assignment. RESULTS: Furosemide shortened the time to left ventricular dysfunction (35.1 +/- 5.1 days in placebo versus 21.4 +/- 3.2 days for furosemide animals; p = 0.038, log-rank test). By day 14, aldosterone levels were significantly higher in furosemide animals (43.0 +/- 11.8 ng/dl vs. 17.6 +/- 4.5 ng/dl; p < 0.05). Serum sodium was reduced (133.0 +/- 0.9 mmol/l furosemide vs. 135.7 +/- 0.8 mmol/l placebo; p < 0.05), but no difference in norepinephrine, potassium, magnesium, creatinine, or urea nitrogen was present. Basal sodium-calcium exchanger currents were significantly increased and isoproterenol responsiveness depressed by furosemide. CONCLUSIONS: Tachycardic pigs given furosemide had significant acceleration of both contractile and metabolic features of CHF, including left ventricular systolic dysfunction, elevated serum aldosterone levels, and altered calcium handling in a controlled experimental model of heart failure.

Adrenergic beta-Agonists↗

PubMed2001

Natural history of hypertrophic cardiomyopathy: Japanese experience.

BACKGROUND AND OBJECTIVES: Most patients with hypertrophic cardiomyopathy (HCM) remain clinically stable for long periods of time, whereas some patients progress to severe systolic dysfunction. Therefore, the natural history of HCM is largely unknown. METHODS: The present study followed up 59 patients with HCM (32 males, 27 females, mean age 38.6 +/- 13.6 years) for 10 years or more (mean 16.0 +/- 4.7 years) after the initial diagnosis. RESULTS: Eight of 17 patients who showed abnormal Q-waves at the initial examination had lost Q-waves, suggesting remodeling from asymmetric to generalized hypertrophy. The thickness of the interventricular septum showed remarkable changes, increasing by > or = 5 mm in 7 patients and decreasing by > or = 5 mm in 21. These observations indicate that ventricular remodeling occurs in patients with HCM. Follow-up electrocardiography demonstrated new Q-waves in 10 patients and bundle branch blocks or intraventricular conduction disturbances in 13. Left ventricular end-diastolic diameter increased from 41.6 to 48.1 mm, associated with a decrease in fractional shortening from 40.6% to 34.0%. Left ventricular systolic dysfunction, defined as left ventricular end-diastolic diameter > 55 mm or fractional shortening < 25%, developed in 13 patients. These observations indicate that myocardial disease including the conduction system is progressive in patients with HCM and finally deteriorates to systolic dysfunction. Left ventricular outflow obstruction also presented evolutional changes. At the initial study, 23 patients showed systolic anterior motion of the mitral valves. Systolic anterior motion disappeared in 13 patients, reduced in 2, increased in 2, and remained stable in only 6. One patient without systolic anterior motion at the initial study developed new systolic anterior motion. Impaired left ventricular filling increased left atrial diameter from 35.5 to 46.9 mm and atrial fibrillation frequently developed (24 patients). CONCLUSIONS: These findings suggest that HCM is a slowly progressive disease which develops evolutional remodeling of left ventricular hypertrophy and outflow obstruction, eventually progressing to systolic dysfunction with cavity dilation and wall thinning.

Adult↗

PubMedDate not supplied

Evaluation of enalapril+losartan treatment with cardiopulmonary exercise test in patients with left ventricular dysfunction.

The aim of this study was to evaluate the effects of the combination of enalapril and losartan in patients with left ventricular systolic dysfunction by means of cardiopulmonary exercise test (CPET). Patients with left-ventricular systolic dysfunction and ejection fractions of 40% or less were included to the study. All patients were under the treatment of enalapril 20 mg once daily. The study group consisted of 20 patients (18 men, 2 women; mean age +/- standard deviation: 62.4 +/-6.5 years) and the comparison group consisted of 10 (8 men, 2 women; mean age 59.3 +/-11.9 years). The dose of 50 mg of losartan once daily was given additionally to the study patients. Breath-by-breath CPET was performed before administration of losartan and then 6-8 weeks later in the study group and 2 times with an interval of 6-8 weeks in the control group without any change in the treatment protocol. In the study group the average exercise times were 361 +/-192 and 454 +/-205 seconds (p = 0.001) before and after the study. Peak oxygen consumption ( VO2) values were 1,209 +/-366 and 1,284 +/-398 mL/minute before and after the study (p = 0.01). Anaerobic threshold VO2 values were 785 +/-187 and 855 +/-217 mL/minute before and after the study, respectively (p = 0.01). Peak heart rates (HR) were 141 +/-28 and 143 +/-22/minute (p = 0.35); peak VO2/HR values were 9.02 +/-3.1 and 9.3 +/-3 mL/minute (p = 0.4) before and after the study, respectively. On the other hand, in the control group, average exercise times were 556 +/-250 and 528 +/-251 seconds (p = 0.8); peak VO2 values were 1,502 +/-537 and 1,450 +/-501 mL/minute (p = 0.2); and anaerobic threshold VO2 values were 1,005 +/-338 and 975 +/-319 mL/min (p = 0.7), before and after the study respectively. At the highest comparable exercise stage for both tests in the study group the expired volume/oxygen consumption ( VE/ VO2) ratio declined from 35.1 +/-6.2 to 32.4 +/-5.6 (p = 0.007). VE values declined from 37.5 +/-10.9 to 33.9 +/-10.1 L (p = 0.02); heart rate declined from 140 +/-27 to 132 +/-21/minute (p = 0.02). No significant change was observed in the mentioned values for the control group. Addition of losartan to the standard therapy in patients with left ventricular systolic dysfunction improved exercise capacity and caused lower heart rate and ventilation requirements for the same exercise level.

Anaerobic Threshold↗

PubMed2000

Heart failure with preserved LV function: pathophysiology, clinical presentation, treatment, and nursing implications.

The syndrome of congestive heart failure occurring secondary to diastolic dysfunction accounts for the major pathophysiologic mechanism in up to one-third of patients who present with dyspnea on exertion and pulmonary congestion. Diastolic dysfunction is characterized by an alteration in the normal diastolic pressure-volume relationship while systolic function may be normal. It is manifested by impairment in the left ventricle's ability to relax and fill completely during diastole at normal low ventricular pressures. This subset of heart failure is most commonly associated with concentric left ventricular hypertrophy and ischemic states. Symptom presentation is similar to that associated with systolic dysfunction as are rates of rehospitalization. Diagnosis is made based on data obtained from invasive and noninvasive procedures. Unlike in the setting of systolic dysfunction, however, there are no large-scale randomized clinical trials evaluating drug efficacy that could be used to guide treatment for the management of diastolic dysfunction. Treatment recommendations, therefore, are empiric. Identifying and aggressively treating potentially reversible causes is a priority. Many of the same drugs used in the management of heart failure associated with systolic dysfunction are also used in the setting of diastolic impairment; however, dosages and rationale for administration may differ. Nursing interventions too are similar. Monitoring response to medications, especially in the acute setting, and comprehensive patient education are paramount. Much is yet to be learned about the management of diastolic dysfunction.

Cardiovascular Agents↗

PubMed2005

[Effects of glutamine on alpha-sarcomeric actin and its mRNA expression of myocardium in rats with endotoxemia].

OBJECTIVE: Endotoxemia is a serious syndrome resulting in multi-organ failure. Once it happens, the penetration of small intestine epithelium increases, body liquid losses, then effective circulating blood decreases and serious metabolic acidosis, serious hypotension, systolic failure, and even shock may occur. In this pathological process, endotoxin, tumor necrosis alpha and systolic dysfunction play important roles. Nowadays, many studies have been done to resolve the systolic dysfunction, but too much attention had been paid to the followings: the depressions of myocardium caused by tumor necrosis alpha, other inflammatory factors, endotoxin and metabolic acidosis; the disturbance of blood vessel-nerve regulations; nitric oxide (NO)/inducible nitric oxide synthase (iNOS) over-synthesis and the decreased density of beta-receptors in the myocardium and/or their activities. Little attention has been paid to the relationship between alpha sarcmeric actin (alpha-SA) and systolic dysfunction during endotoxemia. Glutamine (Gln) can be metabolized into glutathione, an eliminator of free radical. It has been used in preventing myocardial damage from reperfusion. This study aimed to observe the dynamic changes of alpha-SA and mRNA expressions in rats with endotoxemia and examine the effects of Gln on them. METHODS: Classical rat model of endotoxemia was established by intraperitoneal injection of LPS (4 mg/kg, Escherichia coli O55:B5, Sigma). 121 Wistar 18-day-rats were divided into three groups randomly, (1) 0 h control group (normal saline: 1 ml/kg, n = 11). (2) LPS group (LPS: 4 mg/kg, n = 55). (3) Gln group (LPS: 4 mg/kg and immediately 13.64%; Gln: 1 ml/kg, Fresenus, n = 55), Furthermore, LPS and Gln groups were divided into 2, 4, 6, 24 and 72 h time points (n = 11). Each time point of LPS and Gln as well as control rats were anaesthetized at each time point with 1% chloral hydrate injected intraperitoneally at the dosage of 1 ml/kg. Then rats were sacrificed at appoint time, and the hearts were isolated. Eight of them were put in 76 degrees C liquid nitrogen and then frozen in minute 80 degrees C icebox in order to measure the expression of alpha-SA mRNA by RT-PCR. Three of them were fixed in 4% formaldehydum polymerisatum for 12 to 16 h, then the expression of alpha-SA was detected by immunohistochemistry. RESULTS: (1) Compared to 0 h, the expressions of alpha-SA and mRNA in LPS group were significantly depressed (P < 0.01). In LPS group, the lowest was at 6 - 24 h, while in Gln group, it was postponed to 24 h. At 72 h, there was no difference in expressions of alpha-SA between Gln and 0 h group (P > 0.05). (2) Comparing at same time point, the expressions of alpha-SA were significant higher in Gln group than those in LPS group, while the expressions of alpha-SA mRNA in Gln group were high at 4-72 h. There was, however, no significant difference at early phase (P > 0.05). CONCLUSION: Alpha-SA and its mRNA expression were depressed in LPS-induced endotoxemia, especially from 6 to 24 h. It could damage the systolic function. alpha-SA decrease in endotoxemia was due to the inhibited synthesis other than the promoted degradation. Glutamine could inhibit the effects of LPS on both alpha-SA and its mRNA expressions.

Actins↗

PubMed1991

Chronic aortic and mitral regurgitation. Choosing the optimal time for surgical correction.

Valvular surgery for chronic aortic and mitral regurgitation is indicated when symptoms of congestive heart failure have advanced to New York Heart Association class III or when definite and reproducible evidence of left ventricular systolic dysfunction has developed, even in the absence of severe or limiting symptoms. The presence of left ventricular systolic dysfunction can be detected using both invasive and noninvasive measurements of left ventricular end systolic volume (or dimension), end systolic wall stress, and ejection fraction (or fractional shortening). Post-operative results can be optimized when corrective surgery is performed before or soon after the development of left ventricular systolic dysfunction or the development of advanced symptoms.

Aortic Valve Insufficiency↗

PubMed1995

An echocardiographic evaluation of patients with idiopathic heart failure.

The primary myocardial disease idiopathic dilated cardiomyopathy (IDCM) is not clearly defined in the literature. The description is both morphologic and etiologic. We examined consecutive patients with congestive heart failure (CHF) of unknown cause to identify possible cases of IDCM and to give a detailed description of echocardiographic data and possible diastolic dysfunction in this group. The hospital records of patients aged 16 to 65 years hospitalized due to CHF or IDCM during a 6-year period (N = 2,711) were evaluated in a defined region of western Sweden. Twenty-two percent (584/2,711) of these records contained no plausible cause of CHF or IDCM, and among patients being alive, obvious cause was lacking in 411 of 1,516 (27%). These 411 patients were offered a diagnostic investigation, including echocardiography, and they were compared with a randomly selected control group (n = 103) from the general population. Of 411 patients, 293 accepted investigation. From the control group, we defined the reference level for left ventricular (LV) dilatation to be > 32 mm/m2, and reduced ejection fraction according to Teichholz formula to be < 50%. Applying these borderlines, we identified LV dilatation and systolic dysfunction to be present in 30%, either dilatation or systolic dysfunction in 36%, and neither in 34%. In patients without any signs of systolic dysfunction 44% (26/59) showed signs of diastolic dysfunction. In a multivariate analysis, LV dimension was not independently correlated to disease, although LV dimension was univariately correlated to ejection fraction (EF) (r = -0.59; p < 0.0001). However, EF (p < 0.0001), left atrial dimension (p < 0.0001), and the first third filling fraction (p < 0.0001) were the constellation of parameters that most accurately separated patients from controls. By using these three parameters, a positive and negative predictive accuracy of 98% and 61%, respectively, was achieved. Thus, in a consecutive group of patients with idiopathic CHF recruited from a nonselected group of hospitalized patients with CHF, all grades of ventricular function were found. In this group, 30% were identified as having IDCM. We give reference values for the diagnosis of idiopathic IDCM and a simple tool to identify patients with systolic and diastolic dysfunction.

Adult↗

PubMed1978

Effect of digoxin and diuretics on high altitude left ventricular dysfunction.

Systolic time intervals, stroke volume, cardiac output and (dZ/dt)/RZ index were serially estimated in 51 normal healthy volunteers at sea level, for ten days after air induction to 3658 m altitude and on return to sea level. The subjects were divided into three groups and were administered a diuretic, beta methyldigoxin and placebo in a double blind protocol. The group on placebo showed an increase in heart rate, reduction in stroke index and cardiac index during high altitude exposure with normalization on return to sea level. A deterioration in left ventricular function as manifested by prolongation of pre-ejection period, increase in PEP/LVET ratio, reduction in (dZ/dt)/RZ index and left ventricular ejection time was also noted at high altitude. The subjects on digoxin maintained normal stroke/cardiac index and did not show any significant changes in the parameters of myocardial function. The diuretic group showed more deterioration in the parameters than the placebo group. No significant side effects were noted. Left ventricular dysfunction and reduction of stroke index at high altitudes may be causually related; digoxin administration may prevent them from occurring.

Adult↗