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PubMed2001

Mortality and readmission of hospitalized patients with congestive heart failure and preserved versus depressed systolic function.

Patients with congestive heart failure (CHF) and preserved systolic function are very common. Despite the high prevalence of this syndrome, very little information is known regarding its mortality and morbidity (e.g., readmission), or the efficacy of drugs. The purpose of this study was to compare the clinical characteristics and prognosis among consecutively hospitalized patients with CHF and preserved versus depressed left ventricular systolic function. Patients with severe aortic or mitral valve disease were excluded from the study. Patients were categorized based on the values of ejection fraction (EF) as having "preserved" (EF>50%), "intermediate" (EF 40% to 50%), or "depressed" (EF<40%) systolic function. Clinical characteristics as well as mortality and hospital readmission rates during 2.4 years of follow-up were recorded for each patient. Sixty-one patients (35%) had preserved systolic function, 73 (43%) had depressed function, and 38 (22%) had intermediate function. Patients with preserved systolic function were more often women and had a higher prevalence of left ventricular hypertrophy (all p <0.05). At follow-up, cumulative survival probabilities were similar between patients with preserved systolic function and those with systolic dysfunction (p = 0.84). Readmission rates were also comparable between preserved and depressed systolic function (36% vs 48%; p = NS). The prognosis of CHF patients with preserved systolic function was similar to those with systolic dysfunction. In light of these findings, effective therapeutic strategy for this subset of patients is needed.

Aged↗
PubMed2001

Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome.

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.

Cardiomyopathies↗
PubMed2003

American trypanosomiasis (Chagas' disease): an unrecognised cause of stroke.

BACKGROUND: American trypanosomiasis, known as Chagas' disease (CD) is a major cause of cardiomyopathy in South America. Irreversible damage to the heart can appear 10 to 20 years after chagasic infection. The frequency of cerebrovascular complications in chronic CD is unknown. OBJECTIVES: To describe a group of patients with chronic or latent CD affected by ischaemic stroke and identify predictive variables for stroke in CD patients. PATIENTS AND METHODS: Retrospective case series of stroke patients with CD was studied using a cross sectional, descriptive design. CD was confirmed by positive immunofluorescence and haemaglutination serology. Data were collected on age, sex, vascular risk factors, previous history of CD, diagnostic stroke subtype, electrocardiograph and echocardiography findings. Frequency of vascular risk factors were compared with a control group of 239 non-chagasic stroke patients. RESULTS: 136 consecutive CD stroke patients, mean age 56 years, 72 women and 64 men were identified. Vascular risk factors were observed in 81.6% of CD patients. Hypertension (70.29% versus 51.47%; p=0.0004), diabetes mellitus (15.9% versus 6.61%; p=0.0143), and tobacco use (53.98% versus 30.88%; p=0.00002) were significantly less frequent in the CD stroke group. Cardiomyopathy was significantly higher in CD stroke patients (45.58% versus 24.69%; p=0.00005). Abnormal electrocardiograms was observed in 82% of chagasic patients (right bundle branch block 39.5%, left anterior fascicular block 35.8%). Left ventricle (LV) diastolic dysfunction (61.47%), LV systolic dysfunction (51.18%), congestive cardiomyopathy (29.92%), and apical aneurysm (15.74%) were the most frequent echocardiographic findings. Aetiologies were cardioembolism (52.2%), undetermined (36.76%), atherothrombotic (8.82%), and small vessel stroke (2.2%). A diagnosis of CD was established after presentation with stroke in 38.23% of the patients. CONCLUSIONS: CD should be included in the differential diagnosis of stroke in patients of South American origin.

Brain Ischemia↗
PubMed2006

Profound bioenergetic abnormalities in peri-infarct myocardial regions.

Regions of myocardial infarct (MI) are surrounded by a border zone (BZ) of normally perfused but dysfunctional myocardium. Although systolic dysfunction has been attributed to elevated wall stress in this region, there is evidence that intrinsic abnormalities of contractile performance exist in BZ myocardium. This study examined whether decreases of high-energy phosphates (HEP) and mitochondrial F(1)F(0)-ATPase (mtATPase) subunits typical of failing myocardium exist in BZ myocardium of compensated postinfarct remodeled hearts. Eight pigs were studied 6 wk after MI was produced by ligation of the left anterior descending coronary artery (LAD) distal to the second diagonal. Animals developed compensated LV remodeling with a decrease of ejection fraction from 54.6 +/- 5.4% to 31 +/- 2.1% (MRI) 5 wk after LAD occlusion. The remote zone (RZ) myocardium demonstrated modest decreases of ATP and mtATPase components. In contrast, BZ myocardium demonstrated profound abnormalities with ATP levels decreased to 42% of normal, and phosphocreatine-to-ATP ratio ((31)P-magnetic resonance spectroscopy) decreased from 2.06 +/- 0.19 in normal hearts to 1.07 +/- 0.10, with decreases in alpha-, beta-, OSCP, and IF(1) subunits of mtATPase, especially in the subendocardium. The reduction of myocardial creatine kinase isoform protein expression was also more severe in the BZ relative to the RZ myocardium. These abnormalities were independent of a change in mitochondrial content because the mitochondrial citrate synthase protein level was not different between the BZ and RZ. This regional heterogeneity of ATP content and expression of key enzymes in ATP production suggests that energetic insufficiency in the peri-infarct region may contribute to the transition from compensated LV remodeling to congestive heart failure.

Adenosine Diphosphate↗
PubMed2000

Left atrial and ventricular filling in chronic obstructive pulmonary disease. An echocardiographic and Doppler study.

Abnormal left ventricular (LV) diastolic function has frequently been reported in patients with chronic obstructive pulmonary disease (COPD). In the present work, diastolic function was studied by a combined analysis of pulmonary venous and mitral blood flow velocities in 34 patients with COPD clinically stable and without history of heart disease, and 20 control subjects. We confirmed the increased contribution of the atrial contraction to the LV filling in COPD patients in comparison with control subjects; furthermore, a decreased left atrial (LA) filling during the ventricular systole was observed. Changes in LV filling were not the consequence of a systolic dysfunction, because LV systolic function was normal. Doppler indices indicated that LA pressure was below 15 cm H(2)O in all the patients with COPD and control subjects. Several factors can be put forward to explain these changes; the first one is tachycardia. In addition to hypoxemia and medications, echocardiography suggested that a decreased LV preload participated in increased heart rate. Analysis of Doppler transmitral and pulmonary venous flows demonstrated the role of the ventricular interdependence because a correlation existed between LA and LV filling pattern and right ventricle pressure and diameter.

Atrial Function, Left↗
PubMed1998

A truncated cardiac troponin T molecule in transgenic mice suggests multiple cellular mechanisms for familial hypertrophic cardiomyopathy.

Mutations in multiple cardiac sarcomeric proteins including myosin heavy chain (MyHC) and cardiac troponin T (cTnT) cause a dominant genetic heart disease, familial hypertrophic cardiomyopathy (FHC). Patients with mutations in these two genes have quite distinct clinical characteristics. Those with MyHC mutations demonstrate more significant and uniform cardiac hypertrophy and a variable frequency of sudden death. Patients with cTnT mutations generally exhibit mild or no hypertrophy, but a high frequency of sudden death at an early age. To understand the basis for these distinctions and to study the pathogenesis of the disease, we have created transgenic mice expressing a truncated mouse cTnT allele analogous to one found in FHC patients. Mice expressing truncated cTnT at low (< 5%) levels develop cardiomyopathy and their hearts are significantly smaller (18-27%) than wild type. These animals also exhibit significant diastolic dysfunction and milder systolic dysfunction. Animals that express higher levels of transgene protein die within 24 h of birth. Transgenic mouse hearts demonstrate myocellular disarray and have a reduced number of cardiac myocytes that are smaller in size. These studies suggest that multiple cellular mechanisms result in the human disease, which is generally characterized by mild hypertrophy, but, also, frequent sudden death.

Animals↗
PubMed2000

Diastolic dysfunction and heart failure: causes and treatment options.

Diastolic dysfunction is the underlying problem in one third of patients with heart failure, but it is still not well understood. Carefully excluding other causes of heart failure and recognizing indicators of diastolic dysfunction on invasive and noninvasive tests are important in establishing the diagnosis and in guiding therapy. Left ventricular relaxation and stiffness and left atrial function are the most important factors acting together to maintain adequate cardiac output under normal filling pressure. Echocardiography is the most important tool for the diagnosis of diastolic heart dysfunction. It is portable, safe, and excludes other causes of heart failure, such as valvular disease. Diuretics can be used to reduce volume overload, but caution is advised, as aggressive diuresis decreases stroke volume more in diastolic dysfunction than in systolic dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Impact of selective laser ablation of placental anastomoses on the cardiovascular pathology of the recipient twin in severe twin-twin transfusion syndrome.

OBJECTIVES: We investigated the impact of selective laser ablation on the cardiovascular pathology of the recipient twin in twin-twin transfusion syndrome. STUDY DESIGN: Fetal echocardiograms and medical records were reviewed from 22 pregnancies with severe twin-twin transfusion syndrome where echocardiography was performed before and after laser. RESULTS: Before laser, cardiomegaly associated with right and/or left ventricular hypertrophy without ventricular dilatation, was observed in most cases. Right ventricular and left ventricular systolic dysfunction (shortening fraction <28%) was present in 59% and 27%, respectively, and diastolic dysfunction (based on inflow and venous Dopplers) in 73%. Shortly after laser, biventricular systolic function improved significantly and diastolic function tended to improve (50%, P = .06). Functional pulmonary atresia, secondary to right ventricular systolic dysfunction, resolved in 2 of 2 cases at post-laser echocardiography. On serial assessment, diastolic function was normal in 7 of 10, hydrops regressed in 4 of 5, and neither progressive myocardial hypertrophy nor anatomical right ventricular outflow obstruction were found. CONCLUSIONS: Selective laser ablation in severe twin-twin transfusion syndrome acutely improves biventricular systolic function and tends to improve diastolic function in the recipient twin.

Adult↗
PubMed2001

Reduction in myocardial collagen cross-linking parallels left ventricular dilatation in rat models of systolic chamber dysfunction.

BACKGROUND: The transition from compensated left ventricular hypertrophy (LVH) to heart failure is associated with alterations in the myocardial interstitium. We hypothesized that LV dilatation is associated with modifications in collagen cross-linking. METHODS AND RESULTS: We studied 2 rat models of LV dilatation: (1) pressure-overload hypertrophy with heart failure (POH-F) induced by suprarenal abdominal aortic banding and (2) LVH induced by 7 months of isoproterenol (ISO, 0.04 mg x kg(-1) x d(-1)) administration. In POH-F rats and in rats receiving ISO, LV dilatation and a reduced systolic chamber performance were noted. Myocardial hydroxyproline concentrations ([HPRO]) were increased in the POH-F rats, whereas in rats receiving ISO, [HPRO] was decreased. In POH-F rats, the ratio of myocardial collagen type I to type III was increased, but in rats receiving ISO, myocardial collagen I/III was unchanged. In contrast to the diverse changes in myocardial collagen concentrations and phenotypes observed in the 2 models of LV dilatation, the ratio of myocardial insoluble to soluble (relationship between cross-linked and non-cross-linked) collagen was decreased in both the POH-F and ISO groups. Moreover, administration of captopril (0.22 mmol x kg(-1) x d(-1)), which inhibited the ISO-induced reduction in myocardial insoluble/soluble collagen but not the reduction in [HPRO], prevented the ISO-induced alterations in LV dimensions and performance. CONCLUSIONS: Because decreases in the ratio of myocardial insoluble to soluble collagen parallel LV dilatation in rats, reductions in myocardial collagen cross-linking may be an important mechanism contributing to LV dilatation in heart disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Functional relation between infarct thickness and regional systolic function in the acutely and subacutely infarcted canine left ventricle.

Specific information regarding the relation between infarct thickness and regional systolic function is important to the overall understanding of both the pathophysiology of acute and subacute myocardial infarction and the functional benefits of myocardial salvage interventions designed to limit the transmural extent of infarction and thereby preserve left ventricular function. In the present study, quantitative computer-assisted two-dimensional echocardiography was used to define the relation between infarct thickness and systolic function in the acutely and subacutely infarcted canine left ventricle. Echocardiograms were obtained at the mid-papillary muscle level at baseline and 6 h after occlusion (acute infarction) in eight animals and at baseline and 72 h after occlusion (subacute infarction) in nine animals. Systolic function was assessed by measuring the extent of fractional radial shortening along each of 36 evenly spaced endocardial targets from end-diastole to end-systole; the transmural extent of infarction was determined from the triphenyltetrazolium chloride-staining deficit at 6 and 72 h. The relation between systolic function and transmural extent of infarction was analyzed in two ways. First, the extent of fractional radial shortening in each group was examined as a function of quartile (25%) increments in transmural infarct thickness. This analysis revealed 1) a significant overall loss of fractional radial shortening with increasing transmural extent of infarction in both groups; and 2) significant differences in the extent of systolic dysfunction between successive quartile increments of infarction. Second, the relation between infarct thickness and systolic dysfunction was modeled mathematically by fitting the data from each infarct series to linear, logarithmic and exponential functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction. Prognostic indicators.

BACKGROUND: Aortic valve replacement for aortic stenosis (AS) carries an increased risk in the presence of left ventricular (LV) systolic dysfunction. Few data are available on the outcome of such patients. METHODS AND RESULTS: Between 1985 and 1992, 154 consecutive patients (107 men and 47 women) with LV systolic dysfunction (ejection fraction [EF] < or = 35%) underwent aortic valve replacement for AS. The mean preoperative characteristics included EF, 27 +/- 6%; aortic valve mean gradient, 44 +/- 18 mm Hg; aortic valve area, 0.6 +/- 0.2 cm2; and cardiac output, 4.1 +/- 1.5 L/min. Simultaneous coronary artery bypass graft surgery was performed in 78 patients (51%). Perioperative (30-day) mortality was 9% (14 of 154 patients). Fifty patients died during follow-up. Coronary artery disease (P = .002) and a reduced preoperative cardiac output (P = .03) were significantly related to reduced overall survival rate by multivariate analysis. Postoperative improvement occurred in most patients; 88% were New York Heart Association class III or IV before surgery versus 7% after surgery. Postoperative EF was assessed in 76% of survivors; 76% of these demonstrated improvement. By multivariate analysis, change in EF was inversely related to coronary disease (P = .002) and preoperative aortic valve area (P = .03). CONCLUSIONS: Despite LV dysfunction, the risk of aortic valve replacement for AS was acceptable and related to coronary artery disease and mean aortic gradient, and long-term survival was related to coronary disease and cardiac output. Improvement in symptoms and EF occurred in most patients.

Adult↗
PubMed2005

Effects of eplerenone on transcriptional factors and mRNA expression related to cardiac remodelling after myocardial infarction.

OBJECTIVE: To examine the effects of eplerenone, a selective aldosterone blocker, on cardiac function after myocardial infarction (MI) and myocardial remodelling related transcriptional factors and mRNA expression in non-infarcted myocardium. METHODS: MI was induced by ligation of the coronary artery in Wistar rats. Rats were randomly assigned to a vehicle treated group or an eplerenone treated group (100 mg/kg/day). RESULTS: At four weeks after MI, left ventricular (LV) end diastolic pressure, LV weight, and LV end diastolic dimension were increased in MI rats. Eplerenone significantly reduced the increase in LV end diastolic pressure, LV weight, and LV end diastolic dimension. In the MI rats the decreased ejection fraction indicated systolic dysfunction and the increased E wave to A wave ratio and E deceleration rate indicated diastolic dysfunction. Eplerenone significantly attenuated this systolic and diastolic dysfunction. Myocardial interstitial fibrosis, transcriptional activities of activator protein 1 and nuclear factor kappaB, and mRNA expression of monocyte chemoattractant protein 1, plasminogen activator inhibitor 1, atrial natriuretic peptide, brain natriuretic peptide, and collagen types I and III were significantly increased at four weeks after MI. Eplerenone significantly attenuated interstitial fibrosis and suppressed transcriptional activity and mRNA expression of these genes. CONCLUSIONS: When administered after MI, eplerenone prevents cardiac remodelling accompanied by systolic and diastolic dysfunction and inhibits abnormal myocardial transcriptional activities and gene expression.

Animals↗
PubMed1994

Differentiation between systolic and diastolic dysfunction.

Left ventricular (LV) failure can be divided into systolic and diastolic dysfunction. The former is characterized by a reduced ejection fraction and an enlarged LV chamber, the latter by an increased resistance to filling with increased filling pressures. Systolic dysfunction is clinically associated with left ventricular failure in the presence of marked cardiomegaly, while diastolic dysfunction is accompanied by pulmonary congestion together with a normal or only slightly enlarged ventricle. Echocardiography is currently the most relevant technique for non-invasive differentiation of the two forms. Systolic dysfunction is easily assessable by estimation of global ejection fraction and regional wall motion. Diastolic dysfunction can be diagnosed indirectly by means of a normal or nearly normal ejection fraction and and changes of the mitral filling pattern in the context of LV failure. For an exact determination of diastolic dysfunction LV catheterization is required. Systolic dysfunction treatment is well defined, consisting of ACE inhibitors, followed by diuretics and digitalis. Calcium channel blockers are usually contraindicated. Diastolic dysfunction therapy is more dependent on the underlying disease. Calcium channel blockers, ACE inhibitors or beta-blockers are first line drugs in most instances: diuretics can be added with increasing symptoms. Digitalis should be avoided, except in atrial fibrillation, to control heart rate.

Cardiotonic Agents↗
PubMed2005

Left bundle branch block disturbs left anterior descending coronary artery flow: study using transthoracic Doppler echocardiography.

BACKGROUND: This study was performed to evaluate the influence of left bundle branch block (LBBB) on left anterior descending coronary artery (LAD) flow. METHODS: We divided 89 subjects (34 males and 55 females, mean age 64 +/- 14 years) into an LBBB group (n = 40), a right ventricular (RV) pacing group (n = 26), and a control group (n = 23). All of the patients were examined with surface electrocardiography (ECG) and underwent transthoracic Doppler echocardiography (TTE) to measure QRS duration on the ECG, left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), and left ventricular end-systolic volume (LVESV). Coronary flow velocity was measured in the distal LAD with TTE, and the percentage of diastolic flow duration (%DD) was expressed as the percentage of diastolic duration of coronary artery flow divided by the R-R interval. RESULTS: The %DD of the LAD was significantly shorter in the LBBB group (40.4% +/- 12.4%) with LVEF < 50% than in the RV pacing group (60.3% +/- 7.3%) and the control group (59.3% +/- 7.6%) (P < .01 vs the control and RV pacing groups), and it was also significantly shorter in the LBBB group (49.3% +/- 10.5%) with LVEF > or = 50% than in the control and RV pacing groups (P < .01 vs the control and RV pacing groups). In the LBBB group, the %DD of the LAD had a positive correlation with LVEF (P < .05; r = .50), a negative correlation with LVEDV (P < .05; r = -.57), and a negative correlation with QRS duration (P < .05; r = -.41). CONCLUSIONS: Unlike RV pacing, LBBB itself can disturb the coronary perfusion of the LAD through shortening of the diastolic flow duration. Furthermore, systolic dysfunction potentiates the shortening effect of diastolic flow duration by LBBB. Whether left ventricular systolic dysfunction is the result of the coronary flow disturbance by LBBB or vice versa merits further investigation.

Blood Flow Velocity↗
PubMed1999

Blood pressure response to the first 36 hours of heart failure therapy with perindopril versus captopril. French General Hospitals National College of Cardiologists.

An open randomized hospital study conducted in 169 centers in France compared the blood pressure response to the first 36 h of treatment with perindopril (PER), 2 mg once daily, with that to captopril (CAP), 6.25 mg t.i.d., in 725 patients (mean age, 70 years; men, 67%) with echocardiographic left ventricular systolic dysfunction (fractional shortening, < or = 28%) due to ischemia (56.7%) or hypertension (34.5%) and a systolic blood pressure (SBP) > or = 120 mm Hg. Each dose of CAP induced a sharp and rapid decrease in blood pressure (maximum, 1.5-2 h); with PER, the decrease was gradual (maximum, 6 h) and variation was less marked. However, at 36 h, the decrease in blood pressure versus baseline was similar on both treatments. Over the 36-h period, there were 22 (3%) dropouts due to marked orthostatic hypotension (SBP, <90 mm Hg), and they were fewer with PER than with CAP: 16 cases in the CAP group versus six in the PER group (p = 0.036). At 36 h, heart rate was lower with CAP than with PER: 75.2 versus 77.5 beats/min, respectively (p = 0.039). As initial therapy for stabilized left ventricular systolic dysfunction, the first dose of PER (2 mg) induced a significantly smaller decrease in blood pressure than the first dose of CAP (6.25 mg); dropouts due to orthostatic hypotension were also significantly fewer with PER than with CAP.

Aged↗
PubMed1988

Diastolic filling in acute left ventricular dysfunction: role of the pericardium.

Patients with congestive heart failure and elevated left ventricular filling pressures demonstrate an abnormal pattern of diastolic filling that is characterized by a redistribution of diastolic filling to early diastole with reduced reliance on late diastolic filling. The diastolic filling pattern superficially resembles that which is seen with constrictive pericarditis. To examine potential mechanisms for these clinical findings, a model of ischemic left ventricular dysfunction was produced in seven dogs by repeated coronary microsphere embolization, producing a dilated left ventricle with reduced systolic function. Measurements of left ventricular systolic and end-diastolic pressures, rate of rise of left ventricular pressure (dP/dt) and echocardiographic end-diastolic and end-systolic areas were obtained at baseline, during intermediate embolization (moderate left ventricular systolic dysfunction, dilation and mild increases in left ventricular end-diastolic pressure), postembolization (further embolization resulting in severe left ventricular systolic dysfunction, dilation and marked increases in left ventricular end-diastolic pressure), after thoracotomy and after pericardiectomy. The filling fraction at 1/3 and 1/2 of diastole and the time constant of left ventricular pressure decline were also determined. Repetitive coronary microembolization caused progressive left ventricular dilation and decreasing systolic function, which did not change after opening the chest or pericardium. The filling fraction at 1/3 and 1/2 of diastole declined with intermediate embolization (12.0 +/- 5.6% and 23.1 +/- 10.8%, respectively) as compared with baseline values (29.0 +/- 11.9%, 42.9 +/- 15.6%, p less than 0.05). After embolization, there was an increase in the 1/3 and the 1/2 filling fraction (47.5 +/- 8.9%, 72.0 +/- 6.0%, respectively, p less than 0.01) as compared with baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1998

Coronary vasodilator reserve is impaired in patients with hypertrophic cardiomyopathy and left ventricular dysfunction.

BACKGROUND: We tested the hypothesis that a reduced delivery of blood to the myocardium is involved in the development of systolic dysfunction of patients with hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: Eighty-four patients with HCM (62 men, age 43 +/- 12 years) were studied. Left ventricular dimensions and function (fractional shortening) were evaluated by 2-dimensional echocardiography. Myocardial blood flow (MBF) was measured by N13 -ammonia or O15 -water and positron emission tomography at baseline and after dipyridamole; coronary vasodilator reserve (CVR) was calculated as dipyridamole/baseline MBF. Patients with HCM in advanced New York Heart Association (NYHA) classes had lower dipyridamole MBF (NYHA class I = 1.57 +/- 0.64 vs class II = 1.52 +/- 0.58 vs class III = 0.96 +/- 0.32 mL/min per gram; analysis of variance, P <.05) and CVR (NYHA class I = 1.93 +/- 0.64 vs class II = 1.69 +/- 0.54 vs class III = 1.40 +/- 0.43; analysis of variance, P <.05). A positive linear correlation between fractional shortening and dipyridamole MBF was demonstrated (R = 0.23, P <.05), and patients with abnormal fractional shortening had lower dipyridamole MBF (1.07 +/- 0.43 vs 1.58 +/- 0.62 mL/min per gram, P <.01). CONCLUSIONS: Systolic dysfunction in HCM may be caused by a more severe alteration of the coronary vasodilator capacity.

Adult↗
PubMed2002

[Diagnosis of systolic heart failure].

Most of patients with heart failure present a left ventricular systolic dysfunction usually, if not always, associated with a diastolic dysfunction. Clinical manifestations and physical examination allows a presumed diagnosis. Some signs guide toward a systolic heart failure: deviation of cardiac impulse, protodiastolic gallop, functional mitral insufficiency, radiological cardiomegaly associated with signs of postcapillary hypertension, anterior Q wave or complete left bundle branch block. Bed-side dosage of B-type natriuretic peptide is useful to make or exclude the diagnosis of heart failure in patients with acute dyspnea from various causes. Doppler echocardiography is essential to confirm the left ventricular systolic dysfunction and its mechanism: ischemic, valvular or myocardial. The value of shortening fraction is better than eye evaluation. Coronary angiography is indicated when the mechanism of heart failure is unclear and if the patient is relevant to revascularization.

Atrial Natriuretic Factor↗