Prevalence of exercise-induced left ventricular outflow tract obstruction in symptomatic patients with non-obstructive hypertrophic cardiomyopathy.

BACKGROUND: Resting left ventricular outflow tract obstruction (LVOTO) occurs in 25% of patients with hypertrophic cardiomyopathy (HCM) and is an important cause of symptoms and disease progression. The prevalence and clinical significance of exercise induced LVOTO in patients with symptomatic non-obstructive HCM is uncertain. METHODS AND RESULTS: 87 symptomatic patients (43.3 (13.7) years, 67.8% males) with HCM and no previously documented LVOTO (defined as a gradient >or=30 mm Hg) underwent echocardiography during upright cardiopulmonary exercise testing: 54 patients (62.1%; 95% CI 51.5 to 71.6) developed LVOTO during exercise (latent LVOTO); 33 (37.9%; 95% CI 28.4 to 48.5) had neither resting nor exercise LVOTO (non-obstructive). Patients with latent LVOTO were more likely to have systolic anterior motion of the mitral valve (SAM) at rest (relative risk 2.1, 95% CI 1.2 to 3.8; p = 0.01), and higher peak oxygen consumption (mean difference: 10.3%, 95% CI 2.1 to 18.5; p = 0.02) than patients with non-obstructive HCM. The only independent predictors of Delta gradient during exercise were a history of presyncope/syncope, incomplete/complete SAM at rest and Wigle score (all p<0.05). Subsequent invasive reduction of LVOTO in 10 patients with latent obstruction and drug refractory symptoms resulted in improved functional class and less syncope/presyncope (all p<0.05). CONCLUSIONS: Approximately two-thirds of patients with symptomatic non-obstructive HCM have latent LVOTO. This study suggests that all patients with symptomatic non-obstructive HCM should have exercise stress echocardiography.

Steady-state measurement of NO and CO lung diffusing capacity on moderate exercise in men.

Using a rapidly responding nitric oxide (NO) analyzer, we measured the steady-state NO diffusing capacity (DL(NO)) from end-tidal NO. The diffusing capacity of the alveolar capillary membrane and pulmonary capillary blood volume were calculated from the steady-state diffusing capacity for CO (measured simultaneously) and the specific transfer conductance of blood per milliliter for NO and for CO. Nine men were studied bicycling at an average O(2) consumption of 1.3 +/- 0.2 l/min (mean +/- SD). DL(NO) was 202.7 +/- 71.2 ml. min(-1). Torr(-1) and steady-state diffusing capacity for CO, calculated from end-tidal (assumed alveolar) CO(2), mixed expired CO(2), and mixed expired CO, was 46.9 +/- 12.8 ml. min(-1). Torr(-1). NO dead space = (VT x FE(NO) - VT x FA(NO))/(FI(NO) - FA(NO)) = 209 +/- 88 ml, where VT is tidal volume and FE(NO), FI(NO), and FA(NO) are mixed exhaled, inhaled, and alveolar NO concentrations, respectively. We used the Bohr equation to estimate CO(2) dead space from mixed exhaled and end-tidal (assumed alveolar) CO(2) = 430 +/- 136 ml. Predicted anatomic dead space = 199 +/- 22 ml. Membrane diffusing capacity was 333 and 166 ml. min(-1). Torr(-1) for NO and CO, respectively, and pulmonary capillary blood volume was 140 ml. Inhalation of repeated breaths of NO over 80 s did not alter DL(NO) at the concentrations used.

Utility of metabolic exercise testing in distinguishing hypertrophic cardiomyopathy from physiologic left ventricular hypertrophy in athletes.

OBJECTIVES: This study evaluated the role of metabolic (cardiopulmonary gas exchange) exercise testing in differentiating physiologic LVH in athletes from HCM. BACKGROUND: Regular intensive training may cause mild increases in left ventricular wall thickness (LVWT). Although the degree of left ventricular hypertrophy (LVH) is typically less than that seen in hypertrophic cardiomyopathy (HCM), genetic studies have shown that a substantial minority of patients with HCM have an LVWT in the same range. The differentiation of physiologic and pathologic LVH in this "gray zone" can be problematic using echocardiography and electrocardiography alone. METHODS: Eight athletic men with genetically proven HCM and mild LVH (13.9 +/- 1.1 mm) and eight elite male athletes matched for age, size and LVWT (13.4 +/- 0.9 mm) underwent symptom limited metabolic exercise stress testing. Peak oxygen consumption (pVO2), anaerobic threshold, oxygen pulse and respiratory exchange ratios were measured in both groups and compared with those observed in 12 elite and 12 recreational age- and size-matched athletes without LVH. RESULTS: Elite athletes with LVH had significantly greater pVO2 (66.2 +/- 4.1 ml/kg/min vs. 34.3 +/- 4.1 ml/kg/min; p < 0.0001), anaerobic threshold (61.6 +/- 1.8% of the predicted maximum VO2 vs. 41.4 +/- 4.9% of the predicted maximum VO2; p < 0.001) and oxygen pulse (27.1 +/- 3.2 ml/beat vs. 14.3 +/- 1.8 ml/beat; p < 0.0001) than individuals with HCM. A pVO2 >50 ml/kg/min or >20% above the predicted maximum VO2 differentiated athlete's heart from HCM. CONCLUSIONS: Metabolic exercise testing facilitates the differentiation between physiologic LVH and HCM in individuals in the "gray zone."

A prospective randomized trial of complete atrioventricular transplantation versus ventricular transplantation with atrioplasty.

BACKGROUND: The standard technique of ventricular transplantation with atrioplasty (SOHT) distorts atrial anatomy. This may compromise diastolic ventricular function, impair atrioventricular valve competence and elevate resting ANP secretion. In contrast, complete atrioventricular anastomosis (CAVT) preserves atrial geometry. METHODS: We evaluated long term outcome in a prospective randomized trial of CAVT vs. SOHT. The primary outcome measures were peak oxygen uptake, atrioventricular valve regurgitation and ANP secretion. RESULTS: 58 recipients (median age 49 years; range 21-64) were consecutively randomized (29 CAVT; 29 SOHT). There were no differences in total ischaemic time, cardiopulmonary bypass time, postoperative bleeding or immunosuppression. Cardiopulmonary exercise tolerance testing was performed by 29 recipients at 742 to 1825 days. Pulmonary function was equivalent. Peak oxygen consumption expressed as a percentage of predicted maximum was 53.5% with CAVT and 63.8% with SOHT (p = 0.14). Echocardiography was performed on 41 recipients at 944 to 1665 days. There was less tricuspid regurgitation with CAVT (3/22 [13.6%] CAVT vs. 10/19 [52.6%] SOHT; p = 0.019). The incidence of mitral regurgitation was similar (5/22 [22.7%] CAVT vs. 4/19 [21.1%] SOHT; p = 0.803). Resting ANP secretion was assessed in 17 recipients at 1013 to 1812 days. All were hemodynamically stable and none had concurrent rejection. Resting ANP secretion was less with CAVT (CAVT: 283 pg/ml; SOHT: 521.4; p = 0.041). CONCLUSIONS: Peak oxygen consumption was not influenced by implantation technique. However, CAVT reduced the incidence of tricuspid regurgitation and attenuated the elevation in resting ANP secretion.

Effect of exercise training programme on bone mineral density in novice college rowers.

Exercise has important effects on skeletal mineralization. Changes in bone mineral density (BMD) and bone mineral content (BMC) as measured by dual energy X-ray absorptiometry were investigated in a group of 17 male novice college oarsmen over a 7-month period and were compared with eight age-matched controls. The rowing training programme consisted of approximately 8 h rowing, 1 h weight training, and 1 h running per week. After 7 months training the mean BMD of the lumbar spine (L1-L4) had increased significantly by 2.9% (P < 0.001) and the mean BMC had increased by 4.2% (P < 0.001). There was no significant change in the control group. Neither group showed a significant change in BMD or BMC in the femoral neck, greater trochanter or Ward's triangle. This study provides further evidence that exercise plays an important role in bone mineral formation.

Mixed expired nitric oxide in primary pulmonary hypertension in relation to lung diffusion capacity.

The mixed expired nitric oxide (NO) production of the lungs of patients with primary pulmonary hypertension (PPH) and normal subjects was measured to determine the relationship between NO production and the diffusion capacity of the lung (KCO). Expired air was collected from eight patients with PPH and 20 healthy volunteers for analysis by a chemiluminescent analyser. Mean pulmonary artery pressure in the PPH patients was 59.5 +/- 6.45 mmHg and their mean cardiac output was 2.95 +/- 0.35 l/min. All patients and subjects underwent measurements of FEV1, VC and KCO. The rate of production of NO in mixed exhaled air was lower in the PPH group compared to the controls (2.85 +/- 0.7 vs. 4.69 +/- 0.35 nM/min; p < 0.05). There was a good correlation of expired NO with the KCO (r = 0.7; n = 30; p < 0.001). When corrected, KCO differences in exhaled NO were not significant (p = 0.09). We conclude that the low exhaled NO observed in PPH patients is a reflection of the reduced blood capillary volume in these patients rather than a decreased basal production of NO.

The effect of recipient lung size on lung physiology after heart-lung transplantation.

We studied the postoperative course of lung volumes in 32 heart-lung transplant recipients relative to the predicted total lung capacity of the individual donors, to assess the degree of inaccuracy likely to result from the radiological method of matching of donor and recipient lung sizes. There was a tendency for recipients with large preoperative lung volumes--from, for example, emphysema--to receive smaller lungs, while those with smaller volumes from pulmonary vascular disease received bigger donor lungs, but no immediate problems were incurred. After an initial fall in total lung capacity, the postoperative value of the total lung capacity approached the recipients' pretransplant value about one year after the operation irrespective of the size of the donor lungs. This suggests that chest wall compliance is the major determinant of postoperative lung volume and not the donor lung size or compliance. Exact matching of donors' and recipients' lung sizes may not be necessary, and if required can be simply achieved by comparing the measured total lung capacity in the recipient with the predicted value of the donor based on sex, age, and height.