Plasminogen activator inhibitor 1 is elevated in the children of men with premature myocardial infarction.

To assess whether plasminogen activator inhibitor 1 (PAI-1) activity is elevated in the progeny of young coronary men, 193 young subjects were recruited and divided into two groups. Group A consisted of 104 children whose fathers had suffered a myocardial infarction before the age of 55 ("cases"). Eighty-nine young subjects matched for age, sex, body mass index (BMI) and smoking habits without familial history of coronary artery disease (CAD) served as controls (group B). Children with a family history of diabetes mellitus or hypertension were excluded from both groups. We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. PAI-1 activity levels were also determined in the men who suffered a premature myocardial infarction 4 months after their discharge. PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. There was also a positive correlation between PAI-1 activity levels of the affected fathers and their children (r = 0.30, p = 0.01). The present data support the hypothesis that elevated PAI-1 levels in the offspring of men with premature myocardial infarction impair their fibrinolytic capacity contributing to their familial predisposition to CAD.

Comparison of usefulness between exercise capacity and echocardiographic indexes of left ventricular function in cardiac amyloidosis.

In patients with primary systemic amyloidosis (AL), the echocardiographic assessment of ventricular function alone does not always correspond to patients' symptoms and functional status. Peak oxygen uptake and anaerobic threshold (AT), in contrast, constitute 2 objective, reliable and reproducible indicators of functional status in patients with circulatory failure. Thirty-two consecutive patients (mean age 50 +/- 13 years) with histologic evidence of systemic primary AL were studied (29 AL, 3 hereditary). There were 16 with echocardiographic features of cardiac infiltration (group I) and 16 without (group II). Twenty age- and gender-matched healthy subjects were also studied for comparison. Of the 32 patients, 12 were in New York Heart Association functional class I, 9 were in class II, and 11 were in class III. Each subject underwent 2-dimensional and Doppler echocardiography and cardiopulmonary exercise testing using a modified Bruce protocol. Left atrial (LA), left ventricular (LV) dimensions, wall thickness, and LV fractional shortening, as well as transmitral flow velocities and their E/A ratio were measured. Peak oxygen consumption (VO2max [ml/kg/min]), AT (ml/kg/min), and exercise duration (seconds) were also measured. VO2max and AT were lower in patients with AL than in controls (20.8 +/- 7.0 vs 35.0 +/- 8.5, p <0.001 and 13.1 +/- 3.7 vs 27.0 +/- 4.2, p <0.001, respectively). As a group, symptomatic patients had lower VO2max, AT, and exercise duration than those without symptoms (17.1 +/- 3.6 vs 27.0 +/- 6.9, p = 0.0001, 11.1 +/- 2.1 vs 16.2 +/- 3.6, p = 0.0001, and 489 +/- 235 vs 843 +/- 197, p = 0.0001, respectively), whereas LV dimensions only showed a small difference (p = 0.03). VO2max, AT, and exercise duration of patients in functional class I were higher than those in functional classes II and III (p = 0.01, p <0.05, and p = 0.007, respectively). Asymptomatic patients had lower VO2max, AT, and exercise duration than controls (p <0.0001). VO2max, AT, and exercise duration were poorly related to LA diameter, LV dimensions, fractional shortening, wall thickness, peak velocities of E and A waveforms, and E/A ratio. Patients with VO2max > 15 ml/kg/min had a better survival than patients with VO2max < 15 ml/kg/min. Thus, in patients with primary systemic AL, cardiorespiratory exercise testing is the preferred way of assessing functional capacity. Echocardiographic Doppler indexes at rest are not predictive of a patient's symptoms and exercise capacity. Furthermore, VO2max is a strong independent predictor of survival in these patients.

Echocardiographic features of left atrium in elite male athletes.

In athletes, an increase in left atrial volumes is observed, associated with decreased atrial contractile performance and enhanced conduit function.

Effect of atrial fibrillation on exercise capacity in mitral stenosis.

To determine the preoperative and postoperative effect of atrial fibrillation (AF) on exercise capacity in mitral stenosis, 12 digitalized patients in AF (7 women and 5 men, age 52 +/- 6.1 years) and 10 in sinus rhythm (5 women and 5 men, age 46 +/- 5 years) underwent maximal cardiopulmonary exercise testing according to Weber's protocol and Doppler echocardiographic examination before and at 3 and 6 months after mitral valve replacement. The ratio of right ventricular acceleration to ejection time was used as an estimate of mean pulmonary artery pressure. Preoperative exercise duration (6.8 +/- 1 vs 8 +/- 2 minutes), peak oxygen consumption (9.7 +/- 3 vs 12.3 +/- 3 ml/kg/min), and right ventricular acceleration to ejection time ratio (0.34 +/- 0.07 vs 0.34 +/- 0.08) were not significantly different between patients with AF and those in sinus rhythm. Postoperative improvement in these parameters was lower in patients with AF than in those in sinus rhythm: exercise duration at 3 months, 7.5 +/- 2 vs 11.9 +/- 2 minutes (p < 0.001); at 6 months, 9 +/- 2 vs 12 +/- 2 minutes (p < 0.001); peak oxygen consumption at 3 months, 10.8 +/- 3 vs 17.5 +/- 3 ml/kg/min (p < 0.001); and at 6 months, 11.9 +/- 3 vs 17.8 +/- 3 ml/kg/min (p < 0.001); right ventricular acceleration to ejection time ratio at 3 months, 0.35 +/- 0.08 vs 0.42 +/- 0.05 (p < 0.05); and at 6 months, 0.38 +/- 0.05 vs 0.44 +/- 0.05 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Left atrial mechanical function in the healthy elderly: new insights from a combined assessment of changes in atrial volume and transmitral flow velocity.

To assess left atrial mechanical function in the elderly, 35 old (age > 70 years) and 18 sex-matched young (age < 50 years) healthy subjects were studied. Transmitral flow velocities were recorded with pulsed Doppler echocardiography. Left atrial volumes were measured echocardiographically at mitral valve opening (maximal) and closure (minimal) and at onset of atrial systole (P wave of the electrocardiogram) according to the biplane area-length method. Left atrial passive emptying was assessed with the passive emptying volume (maximal-volume at onset of atrial systole) and fraction (passive emptying volume/maximal). Left atrial active emptying was assessed with the active emptying volume (volume at onset of atrial systole-minimal) and fraction (active emptying volume/volume at onset of atrial systole) and with left atrial ejection force = 0.5.blood density.volume at onset of atrial systole.active emptying fraction.(A velocity)2/A integral. Left atrial volumes were greater in old compared with young subjects (maximal: 31 +/- 10 cm3/m2 vs 24 +/- 8 cm3/m2, p = 0.02; at onset of atrial systole: 23 +/- 8 cm3/m2 vs 15 +/- 5 cm3/m2, p = 0.0002; minimal: 13 +/- 5 cm3/m2 vs 9 +/- 4 cm3/m2, p = 0.001). Passive emptying volume and fraction were lower (7.8 +/- 1.7 cm3/m2 vs 9.2 +/- 3.2 cm3/m2 [p = 0.04] and 26.4% +/- 9.8% vs 37.9% +/- 11.2% [p = 0.003], respectively), whereas atrial ejection force and active emptying volume were greater in old compared with young subjects (6.8 +/- 3.3 kdynes/m2 vs 4.2 +/- 2.8 kdynes/m2 [p = 0.007] and 9.2 +/- 4.1 cm3/m2 vs 5.7 +/- 2.9 cm3/m2 [p = 0.002], respectively). The active emptying fraction was similar in the two groups (39.7% +/- 11% vs 38.4% +/- 13%; difference not significant). Thus advanced age is associated with depressed left atrial passive emptying function and increased left atrial volume. Left atrial dilation contributes to an increase in atrial ejection force and the amount of blood ejected during left atrial systole and may represent an important compensatory mechanism in this age population.

Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes.

One of the targets of anti-hypertensive treatment is cardiovascular structural and functional improvements, while the level of blood pressure (BP) under treatment is related to patient morbidity and mortality. The aim of this study was to evaluate the relation of BP achieved after felodipine monotherapy to the degree of cardiovascular changes. Six hundred patients with essential hypertension were studied and grouped according to diastolic BP (DBP) levels after 6 months of therapy: 90-94 (n = 86), 85-89 (n = 186), 80-84 (n = 180) and < 80 mm Hg (n = 148). Overall BP fell from 175/103 to 137/83 mm Hg with a concomitant moderate reflex tachycardia (3.3%). Left ventricular (LV) dimensions decreased to a degree (-0.4 and -0.8%, P < 0.0001), with the greatest decrease in patients with lower DBP levels under treatment (P < 0.0001). LV systolic function improved to a modest degree (0.8%, P < 0.0001), depending on DBP fall (P < 0.0001), as did cardiac output (2.4%, P < 0.0001). LV systolic wall stress and total peripheral resistance fell (-18% and -14%, P < 0.0001) in relation to DBP drop (P < 0.0001), as did aortic root distensibility (55%, P < 0.0001). It is concluded that the degree of cardiovascular structure and function improvements are directly related to the DBP levels achieved under felodipine anti-hypertensive therapy.

An unusually hard lesion in an aortocoronary saphenous vein graft refractory to standard balloon angioplasty.

We report a case of a hard lesion in the body of an aortocoronary saphenous vein graft, which developed 3 years after bypass surgery and was not amenable to dilation during percutaneous coronary angioplasty, despite multiple balloon inflations at pressures reaching 13 atm. Hard lesions in aortocoronary saphenous vein grafts are rare but may lead to balloon angioplasty failure necessitating alternative angioplasty options.

Relation of left atrial volume and systolic function to the hormonal response in idiopathic dilated cardiomyopathy.

We studied the relation of left atrial mechanical function to the hormonal response in 14 patients with idiopathic dilated cardiomyopathy. Left atrial volumes were echocardiographically measured at mitral valve opening (maximal), at onset of atrial systole (onset of the P wave of the electrocardiogram) and at mitral valve closure (minimal) from the apical 2- and 4-chamber views using the biplane area-length method. Left atrial systolic function was assessed with the left atrial active emptying fraction ([volume at onset of atrial systole-minimal]/[volume at onset of atrial systole]). Plasma renin activity, aldosterone and atrial natriuretic peptide plasma levels were determined using commercially available kits. Left atrial maximal volume was directly, and left atrial active emptying fraction was inversely related to plasma renin activity (r = 0.60, P = 0.02 and r = -0.59, P = 0.026, respectively), aldosterone (r = 0.61, P = 0.02 and r = -0.53, P = 0.048) and atrial natriuretic factor (r = 0.79, P = 0.0009 and r = -0.62, P = 0.01) plasma levels. Thus, increased left atrial size and depressed left atrial contractile performance are associated with increased hormonal response in idiopathic dilated cardiomyopathy.

Coronary artery disease: changes of blood lymphocyte subsets induced by physical exercise.

To examine the changes in the absolute numbers of blood lymphocyte subsets in patients with coronary artery disease, we studied 26 patients with documented coronary artery disease (group I) and 15 other subjects (group II) with atypical complaints and negative exercise test who served as controls. Blood lymphocyte subsets were determined at rest, immediately and 24 h after a bicycle exercise test. In both groups the absolute number of leukocytes/mm3 and lymphocytes/mm3 was significantly greater immediately after exercise than at rest and returned to baseline values by 24 h post-exercise. The absolute number of B-lymphocytes and CD8+ T-lymphocytes did not change significantly in both groups, while CD3+ and CD4+ T-lymphocytes as well as CD25+ activated T-lymphocytes declined insignificantly immediately after exercise but increased significantly 24 h after exercise in both groups, with a higher increase (P<0.01) in all three variables under study (CD3+, CD4+ and CD25+ T-lymphocytes) in group I in comparison to group II (P<0.05). Our findings showed that changes in lymphocyte subsets induced by physical exercise differ between patients with and without documented coronary artery disease, suggesting that an alteration in immune function may account for these differences.

Chemokines in patients with ischaemic heart disease and the effect of coronary angioplasty.

Percutaneous coronary transluminal angioplasty (PTCA) may release inflammatory mediators such as chemokines. Monocyte chemoattractant protein-1 (MCP-1) and eotaxin (EOX) are monocyte- and eosinophil-specific chemokines involved in the inflammation and pathogenesis of coronary atherosclerosis. A total of 28 patients undergoing elective PTCA, 20 coronary artery disease (CAD) patients undergoing coronary angiography and 28 healthy controls were studied. In PTCA patients before the procedure, MCP-1 plasma levels (441+/-64 pg/ml) were similar to those of CAD patients (430+/-24 pg/ml), and significantly higher compared with controls (145+/-17 pg/ml, P<0.01). MCP-1 rose significantly after 3 and 6 months following PTCA (696+/-89 and 876+/-86 pg/ml, respectively, P<0.01 vs. before PTCA). EOX plasma levels (155+/-14 pg/ml) were similar to those of CAD patients (157+/-14 pg/ml), but significantly higher compared with controls (83.2+/-10 pg/ml, P<0.05). EOX rose significantly 24 h (273+/-41 pg/ml, P<0.05) but not 3 months after PTCA (160+/-20 and 158+/-19 pg/ml, respectively). These findings indicate that chemokine-induced monocyte- and eosinophil-specific chemoattraction is stimulated in patients with coronary artery disease. MCP-1 levels remain significantly elevated for at least 6 months following elective PTCA, suggesting an inflammatory stimulation.

Left atrial volume and function in valvular aortic stenosis.

To assess left atrial volume and function in aortic stenosis, 20 patients with this condition and 10 normal controls were studied. Atrial volumes were measured by echocardiography at mitral valve opening (maximal), onset of atrial systole (P wave of the electrocardiogram) and mitral valve closure (minimal), using biplane techniques. The maximal volume was greater in those patients with aortic stenosis as compared to the controls (74.8 +/- 26.4 cm3 vs. 46.4 +/- 11.9 cm3, p < 0.005), and was directly related to left ventricular mass (r = 0.77). The passive emptying volume (maximal minus onset of atrial systole) was similar in the two groups (21 +/- 8 cm3 vs. 18.7 +/- 5.9 cm3, p = NS), while active emptying volume (onset of atrial systole minus minimal) was higher in aortic stenosis (16.8 +/- 5.2 cm3 vs. 10.2 +/- 2.5 cm3, p < 0.001). The total emptying volume (sum of passive and active) was slightly higher amongst those with aortic stenosis (37.4 +/- 10.2 cm3 vs. 28.9 +/- 7.5 cm3, p < 0.05). The passive emptying fraction (passive emptying volume/maximal) was lower in the aortic stenosis group (0.28 +/- 0.08 vs. 0.40 +/- 0.05, p < 0.001), while the active emptying fraction (active emptying volume/volume at onset of atrial systole) was similar between the two groups (0.33 +/- 0.09 vs. 0.37 +/- 0.05, p = NS). Increased left atrial size in aortic stenosis is directly related to left ventricular mass and restores left atrial total emptying volume, despite the depressed passive emptying fraction. Left atrial dilatation thus represents an important compensatory mechanism, contributing to the maintenance of left ventricular stroke volume and cardiac output in severe aortic stenosis.

A comparative study of the effect of coronary artery disease on ascending and abdominal aorta distensibility and pulse wave velocity.

UNLABELLED: The effect of coronary artery disease on aortic distensibility and pulse wave velocity was studied in 73 male normotensive patients, divided in two groups. Group A (n = 36) consisted of patients with normal coronaries and one-vessel disease and Group B (n = 37) of patients with two- and three-vessel disease. Distensibility (10(-6).cm2.dyne-1) was calculated from the equation: 2 x [(change in aortic diameter from systole to diastole/(diastolic aortic diameter) x (pulse pressure)]. Aortic diameters were measured with two-dimensional guided M-mode echocardiography. For ascending aorta distensibility calculations, pulse pressure (PP) measured at brachial artery with sphygmomanometry (BrPP) was employed. For abdominal aorta distensibility calculations, BrPP was corrected from the equation: corrected BrPP = 0.642 x BrPP + 42.54 (r = 0.9) obtained by comparing BrPP and abdominal aorta PP measured directly during cardiac catheterization. RESULTS: 1) Ascending and abdominal aorta distensibility were greater in Group A compared to Group B (2.732 +/- 0.92 vs 0.688 +/- 0.57, p < 0.0001 and 2.098 +/- 0.65 vs 0.871 +/- 0.64, p < 0.0001 respectively). Moreover, ascending was greater than abdominal aorta distensibility in Group A (p < 0.0001), while no significant difference between the two was observed in Group B and 2) Pulse wave velocity was inversely related to ascending and abdominal aorta distensibility (r = -0.56 and r = -0.5 respectively). Thus, high grade coronary atherosclerosis is associated with decreased distensibility and loss of elastic inhomogeneity of the aorta resulting in increased pulse wave velocity.

Predictive value of biomarkers in patients with heart failure.

Heart failure (HF) is a complex syndrome with high morbidity and mortality while, myocardial injury, hemodynamic overload, genetic, neurohormonal, inflammatory and biochemical factors are implicated in the development and progression of the disease. Interestingly, despite the development of several diagnostic tests, HF diagnosis remains clinical, based on symptoms and signs, while there is a poor relationship between symptoms and the prognosis of HF. Several biomarkers have recently been examined for their efficacy to predict outcome and assess prognosis of HF patients. The best studied for its prognostic ability sub-group of biomarkers is the neurohormones including the natriuretic peptides, the components of the renin-angiotensin-aldosterone system and the catecholamines. Others sub-groups of biomarkers include inflammatory and oxidative stress markers, extracellular matrix remodeling markers and myocardial injury markers (such as troponins I and T). Nevertheless, it is difficult to access a single biomarker fulfilling our need to evaluate prognosis and guiding treatment in acute or chronic HF patients, thus the predictive ability of combined biomarkers is recently under research. Therefore, further studies are needed to elucidate the clinical significance of these biomarkers. In the present review, we will discuss the usefulness and significance of potentials or established biomarkers in HF patients focusing on their ability to predict adverse events, morbidity and mortality.

Effects of atorvastatin on reactive hyperaemia and the thrombosis-fibrinolysis system in patients with heart failure.

OBJECTIVE: To investigate the effects of short term atorvastatin treatment on forearm vasodilatory response to reactive hyperaemia (RH%) and on components of the thrombosis-fibrinolysis system (antithrombin III, proteins and S, factors V and VII, von Willebrand factor, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1)) in patients with heart failure. PATIENTS AND METHODS: 35 patients with heart failure were enrolled in this study; 17 patients received atorvastatin 10 mg/day and 18 patients received no statin for four weeks. Forearm blood flow (FBF) was measured by venous occlusion strain gauge plethysmography. RH% and forearm vasodilatory response to nitrate were defined as the percentage change of FBF from rest to the maximum flow during reactive hyperaemia and after nitrate administration, respectively. Plasma concentrations of antithrombin III, protein C, protein S, factor V, factor VII, von Willebrand factor, tPA, and PAI-1 were determined before and after treatment. RESULTS: Maximum hyperaemic FBF remained unchanged in both groups. Baseline FBF was slightly but not significantly decreased in the atorvastatin treated group. RH% was significantly increased only in the atorvastatin treated group, from mean (SD) 42.44 (18.9)% to 83.7 (36.1)% (p < 0.01). Plasma concentrations of antithrombin III (from mean (SD) 81.7 (11.37)% to 73.5 (13.8)%), protein C (from mean (SD) 88.3 (26.9)% to 63.9 (25.0)%), factor V (from mean (SD) 126.2 (33.4)% to 94.9 (29.8)%), tPA (from median (25th-75th percentile) 11.68 (8.60-20.95) ng/ml to 10.30 (8.65-15.12) ng/ml), and PAI-1 (from median (25th-75th percentile) 3.10 (2.15-4.40) IU/l to 1.90 (0.75-3.0) IU/l) were significantly decreased in the atorvastatin treated group (p < 0.05) but not in the control group. Plasma concentrations of von Willebrand factor, factor VII, and protein S remained unaffected in both groups. CONCLUSION: Atorvastatin did not change the maximum hyperaemic flow, although it decreased plasma concentrations of antithrombin III, protein C, factor V, tPA, and PAI-1 in patients with heart failure. Therefore, short term treatment with atorvastatin may affect the expression of both endothelium and liver derived components of the thrombosis-fibrinolysis system in patients with heart failure.

Factors affecting the postoperative exercise capacity of patients with mitral stenosis and aortic regurgitation.

Factors affecting the exercise capacity of patients with mitral stenosis (MS) and aortic regurgitation (AR) are incompletely understood. Accordingly, exercise capacity was assessed in 13 patients with MS and in 13 with AR by means of cardiopulmonary exercise testing before as well as 3, 6 and 12 months after valve replacement. Left- and right-ventricular function were evaluated echocardiographically. Both in MS and in AR exercise capacity expressed by maximal oxygen consumption (VO2max) increased significantly after valve replacement and was directly related to right ventricular (RV) function assessed by the ratio of RV acceleration time to RV ejection time (r = 0.87, p < 0.001 and r = 0.74, p < 0.001, respectively) and inversely related to left atrial diameter (r = -0.72, p < 0.001 and r = -0.76, p < 0.001, respectively). No relation between VO2max and resting left-ventricular function was found. Thus, the postoperative improvement in the exercise capacity both in mitral stenosis and in aortic regurgitation is associated with an improvement in right-ventricular function and a decrease in left-atrial size.

Clinical significance of antibodies against tropomyosin, actin and myosin in patients with dilated cardiomyopathy.

In the present study we evaluated the importance of autoimmune mechanisms in dilated cardiomyopathies. Sera from 81 patients with dilated cardiomyopathy, 17 patients with various other cardiologic diseases and 40 apparently healthy blood donors were tested with an immunoassay method for the presence of autoantibodies against tropomyosin, myosin and actin, three antigens which are components of the cardiac tissue. Elevated values of autoantibodies were obtained in a high percentage of patients with dilated cardiomyopathy as compared to the control group (66% antitropomyosin IgG, 66% antimyosin IgG, 28.3% antitropomyosin IgM). It has also been shown, for the first time, that patients with dilated cardiomyopathy and positive for at least one of the screened autoantibodies had a thicker interventricular septum thickness, systolic and diastolic than patients negative for the presence of autoantibodies (1.18 +/- 0.3, 1.2 +/- 0.3 vs 0.88 +/- 0.1, 0.9 +/- 0.2 respectively), a finding that indicates the importance of these autoantibodies. Although further investigation is needed, it is concluded that the detection of these autoantibodies can be a useful tool for the diagnosis, follow-up and prognosis of the patients with dilated cardiomyopathy.

The impact of risk factors for atherosclerosis on the vasomotor effects of inhibition of nitric oxide synthesis in patients with normal angiograms.

We assessed the impact of systematic risk factors on the vasomotor effects of inhibition of nitric oxide synthesis. N(G)-monomethyl-L-arginine (LNMMA) was infused intracoronarily at 4, 8 and 16 micromol/min followed by intracoronary bolus administration of 250 microg nitroglycerin. Computerized angiography was used to assess the changes in the diameter of coronary segments. During the LNMMA infusions there was no significant difference in LNMMA response between smokers and non-smokers (-5.5+/-0.8 and -6.6+/-0.6%, respectively) or between hypertensives and normotensives (-6.4+/-1.1 and -6.1+/-0.6%, respectively), but the response was less in hypercholesterolaemic patients (-4.5+/-0.7 vs. -8.0+/-0.6%, p<0.05). Thus, the reduced nitric oxide activity is related to hypercholesterolaemia but not to smoking and hypertension.

Left atrial myopathy in idiopathic dilated cardiomyopathy.

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

Exercise capacity in patients with beta-thalassemia major: relation to left ventricular and atrial size and function.

OBJECTIVES: The objective of this study was to examine the association between exercise capacity and echocardiographic indexes of atrial and ventricular function and size in patients with beta-thalassemia major. BACKGROUND: In patients with beta-thalassemia major, the assessment of cardiac function with echocardiography alone does not always correspond to their functional status. Peak oxygen uptake and anaerobic threshold, on the other hand, constitute 2 objective and reproducible determinants of exercise capacity in patients with heart failure. METHODS AND RESULTS: Forty consecutive patients (22 women and 18 men, 18 to 30 years old) who were in stable condition while receiving regular transfusions and 30 age- and sex-matched control subjects were studied. At 2 to 3 days after the last transfusion, each subject underwent complete echocardiographic study followed by cardiopulmonary exercise testing. Left atrial volumes (maximal [Vmax], at onset of atrial systolic [Vp], and minimal [Vmin]) and left ventricular volumes were measured with the biplane area-length method, and left atrial active emptying fraction (ACTEF) and left ventricular ejection (LVEF) fraction were calculated. Peak oxygen uptake (Vo 2 max) and anaerobic threshold (AT) were also estimated. After transfusion, patients with beta-thalassemia major had reduced Vo 2 max and AT and greater left atrial volume in comparison with control subjects. Also, ACTEF and LVEF were significantly lower in the patient group. Moreover, Vo2 max and AT were inversely related to Vmax (r = -0.74 and r = -0.80, respectively) and directly related to ACTEF (r = 0.85 and r = 0.82, respectively) in beta-thalassemia major, whereas they were poorly related to LVEF (r = 0.50 and r = 0. 53, respectively). In the control group, Vo 2 max and AT parameters were related to Vmax and ACTEF in a similar way to that in the beta-thalassemia group. CONCLUSIONS: In patients with beta-thalassemia major, exercise capacity does not correlate with left ventricular dimensions and function. On the contrary, left atrial size and systolic dysfunction are probably predictors of decreased exercise capacity.