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The prognostic value of N-terminal proB-type natriuretic peptide.

The heart is not only a pump, but also it is an endocrine organ. Cardiac stretch and overload stimulate the secretion of natriuretic peptides, which have a variety of beneficial actions, such as vasodilation and natriuresis. Cardiac-derived natriuretic peptides, especially B-type natriuretic peptide (BNP), have emerged as useful biomarkers for the diagnosis, and potentially the treatment, of heart failure patients. The inactive amino-terminal fragment of the BNP prohormone (NT-proBNP), which is more stable than mature BNP, has also been recognized as an aid in the diagnosis of left-ventricular systolic dysfunction. Furthermore, elevated NT-proBNP concentrations have been shown to be predictive of poor prognosis in a variety of cardiovascular diseases, suggesting that it could be useful for risk stratification of patients. This review summarizes current literature that has addressed the issue of NT-proBNP as a prognostic tool in heart failure, acute coronary syndromes and other conditions.

Acute Disease↗

Left ventricular function in young adults with childhood and adulthood onset growth hormone deficiency.

OBJECTIVE: The impairment of heart structure and function in adults with childhood onset GH deficiency has been recently described. However, previous echocardiographic studies have reported no differences in cardiac mass and function between adulthood onset GH deficient patients and healthy subjects. DESIGN: The aim of this study was to evaluate cardiac performance in adult patients with childhood and adulthood onset GH deficiency, using equilibrium radionuclide angiography, a method more accurate than echocardiography. PATIENTS: Eleven patients with childhood onset GH deficiency, 9 patients with adulthood onset GH deficiency and 12 age-, gender-, height- and weight-matched healthy subjects entered the study. MEASUREMENTS: All the study population underwent equilibrium radionuclide angiography at rest and during physical exercise. RESULTS: Both childhood and adulthood onset GH deficient patients had an impaired left ventricular systolic performance both at rest (ejection fraction was 55 +/- 6%, 55 +/- 10% and 66 +/- 6% in childhood and adulthood onset GH deficient patients and control group, respectively; P < 0.0001) and during physical exercise (ejection fraction was 54 +/- 9% in childhood onset GH deficient patients, 53 +/- 9% in adulthood onset GH deficient patients and 76 +/- 7% in normal subjects; P < 0.0001). Peak ejection rate was 3.2 +/- 0.8 end-diastolic volume/second, 3.0 +/- 0.6 end-diastolic volume/second and 3.9 +/- 0.8 end-diastolic volume/ second in childhood and adulthood onset GH deficient patients and control group, respectively (P < 0.01). Exercise-induced changes in end-systolic volume were increased in both groups of patients compared with healthy subjects. In contrast, exercise-induced end-diastolic volume changes were not different between GH deficient patients and controls. Resting peak filling rate was 2.6 +/- 0.7 end-diastolic volume/second, 2.5 +/- 0.7 end-diastolic volume/ second and 3.1 +/- 0.3 end-diastolic volume/second in the 2 groups of patients and healthy subjects, respectively (P < 0.05). Reduced exercise tolerance in all patients, as shown by the significantly lower values of peak workload (P < 0.0001), peak rate-pressure product (P < 0.01) and exercise duration (P < 0.0001) was observed. CONCLUSION: Patients affected by GH deficiency have left ventricular systolic dysfunction at rest and during physical exercise, suggesting that GH plays a physiological role in maintaining normal cardiac performance in humans. Furthermore, no difference between childhood and adulthood onset GH deficient patients was found indicating that both group of patients have an impairment of cardiac function.

Adult↗

Congestive heart failure in patients with valvular aortic stenosis. A clinical and echocardiographic Doppler study.

The aim of this study was to evaluate echographically anatomic and functional features of the left ventricle in adult patients with valvular aortic stenosis according to the presence or absence of congestive heart failure and the level of ventricular performance. Fifty-six adult patients with moderate-to-severe aortic stenosis underwent echocardiographic Doppler examination in order to evaluate left ventricular mass and dimensions, systolic function and filling dynamics. Twenty-seven patients had no heart failure and were symptomatic for angina (5), syncope (4) or were symptom-free (group I); the other 29 had heart failure (group II): 16 with normal left ventricular systolic performance (fractional shortening > 25%, group IIa) and 13 with systolic dysfunction (fractional shortening < or = 25%, group IIb). Despite a similar left ventricular mass, compared to group IIa, group IIb showed a significant left ventricular dilatation (end-diastolic diameter: 61 +/- 6.5 vs. 45.5 +/- 6.1 mm, p < 0.001) and mild or no increase in wall thickness (11.5 +/- 1.6 vs. 14.9 +/- 2 mm, p < 0.001). Indices of left ventricular filling on Doppler transmitral flow were also significantly different between the two groups, with a higher early-to-late filling ratio and a shorter deceleration time of early filling in group IIb (2.8 +/- 1.9 vs. 1.2 +/- 0.85, p < 0.01, and 122 +/- 66 vs. 190 +/- 87 ms, p < 0.05, respectively), both indirectly indicating higher left atrial pressure. Finally, heart failure was generally more severe in group IIb patients. In some patients with aortic stenosis, symptoms of heart failure may be present despite a normal left ventricular systolic function and seem to depend on abnormalities of diastolic function. The presence of systolic or isolated diastolic dysfunction appears to be related to a different geometric adaptation of the left ventricle to chronic pressure overload.

Aged↗

Therapy implications of transthoracic echocardiography in acute ischemic stroke patients.

BACKGROUND AND PURPOSE: Stroke is the third leading cause of death in most Western countries. Cardioembolism might be responsible for 15% to 20% of ischemic strokes. Although atrial fibrillation can be diagnosed by electrocardiography, the remaining causes of cardioembolic stroke are diagnosed by echocardiography. Recent recommendations on the management of acute ischemic stroke fail to consider echocardiography as an essential test in all patients. METHODS: We conducted a prospective observational study, performing transthoracic echocardiography on all patients admitted in our hospital with ischemic stroke, in sinus rhythm, from January 7, 2002, to October 16, 2003. Findings compatible with heart diseases that would indicate anticoagulation as beneficial were identified. RESULTS: Of the 853 patients admitted with ischemic stroke, transthoracic echocardiography was performed on 846 (99.2%). Of the 435 patients with ischemic stroke, in sinus rhythm, 37.2% had findings indicating anticoagulation as beneficial: dilated cardiopathy (19.1%), previous anterior wall myocardial infarction (6.2%), left ventricular systolic dysfunction with an ejection fraction <35% (3.7%), mitral valve stenosis with enlarged left atria (1.6%), intracardiac masses (0.5%), valvular prosthesis (0.2%), and >1 abnormality (5.5%). CONCLUSIONS: In our study, transthoracic echocardiography had therapy implications in 37.2% of ischemic stroke patients in sinus rhythm. Transthoracic echocardiography should be considered an essential test in all ischemic stroke patients in sinus rhythm.

Aged↗

Effects of metoprolol in chagasic patients with severe congestive heart failure.

BACKGROUND: Beta-blockers are the most effective and promising treatment for congestive heart failure secondary to left ventricular dysfunction and sympathetic activation. METHODS: Since chagasic patients with severe congestive heart failure have left ventricular systolic dysfunction and neurohormonal activation, we administered metoprolol to nine chagasic patients who were in severe congestive heart failure. Metoprolol (5 mg p.o. daily) was uptitrated on a weekly basis. RESULTS: Patients were receiving digitalis, diuretics and angiotensin converting enzyme inhibitors and had left ventricular dilatation (6.77+/-0.89 cm), depressed ejection fraction (0.20+/-0.06), low systolic blood pressure (93+/-11 mm Hg), sinus tachycardia (115+/-17 beats/min) and sympathetic activation 400+/-246 pg/ml). One patient was in New York Heart Association Functional class III and eight patients were in functional class IV. At the end of the fifth week of treatment (metoprolol 25 mg), seven patients were in functional class III and two were in functional class II. Heart rate decreased to 85+/-15 beats/min (P<0.05) and the systolic blood pressure increased to 108+/-18 mm Hg (P<0.01). There were no significant changes in left ventricular ejection fraction. By the end of the tenth week of treatment (metoprolol 50 mg), four patients were now in functional class I and five were in functional class II. Left ventricular ejection fraction increased to 0.27+/-0.05 (P<0.01) and the left ventricular systolic diameter decreased from 6.38+/-0.90 at baseline to 5.89+/-0.59 and 5.76+/-0.96 after 25 and 50 mg of metoprolol treatment, respectively (P<0.04). Plasma norepinephrine decreased non-significantly to 288+/-91 pg/ml. CONCLUSION: Beta-blockers improve the clinical status and the left ventricular function of chagasic patients with severe congestive heart failure.

Adrenergic beta-Antagonists↗

Revascularization for patients with severe coronary artery disease and left ventricular dysfunction.

Heart failure is becoming increasingly prevalent, and currently coronary artery disease (CAD) is the primary cause of left ventricular (LV) systolic dysfunction. A potential therapeutic option for patients with severe CAD and LV dysfunction is a strategy of revascularization. In this review, we summarize the available literature regarding revascularization for these patients. The literature suggests that patients with severe CAD and LV dysfunction may benefit from revascularization and those patients with viable myocardium may derive the most benefit.

Angioplasty, Balloon, Coronary↗

Aldosterone blockade in post-acute myocardial infarction heart failure.

Development of heart failure (HF) or left ventricular systolic dysfunction (LVSD) significantly increases mortality post acute myocardial infarction (AMI). Aldosterone contributes to the development and progression of HF post AMI, and major guidelines now recommend aldosterone blockade in this setting. However, lack of practical experience with aldosterone blockade may make clinicians hesitant to use these therapies. This review is based on a consensus cardiology conference that occurred in May 2005 (New York City) concerning these topics. Potential barriers to the use of aldosterone blockade are discussed and an algorithm for appropriate in-hospital pharmacologic management of AMI with LVSD and/or HF is presented.

Algorithms↗

Calcium channel blockers for heart rate control in atrial fibrillation complicated by congestive heart failure.

OBJECTIVES: To review the safety and efficacy of verapamil and diltiazem with respect to ventricular response in atrial fibrillation (AF) in the setting of left ventricular (LV) systolic dysfunction. DATA SOURCES: Pertinent articles were identified through a MEDLINE search of the English language literature from 1984 to 1993, followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Studies selected were case reports, controlled trials, review articles and editorials. DATA EXTRACTION: Effects of verapamil and diltiazem on hemodynamics, ventricular response in AF, clinical parameters and mortality were reviewed. DATA SYNTHESIS: There are limited data about the effects of verapamil and diltiazem on ventricular function in patients with congestive heart failure. In vitro diltiazem has fewer negative inotropic effects than verapamil. Clinically there are some reports of hemodynamic and clinical deterioration in patients with significant LV dysfunction given verapamil although most patients improve with verapamil. There are more data concerning diltiazem in the setting of AF complicated by congestive heart failure. The drug does not appear to exacerbate heart failure, although hypotension can result. In chronic AF complicated by heart failure, there is concern that diltiazem may increase mortality. Options for therapy are digoxin, beta-blockers and atrioventricular node ablation. CONCLUSIONS: Calcium channel blockers may have a role in the acute reduction of ventricular response in patients with AF complicated by congestive heart failure; however, their safety in chronic heart rate control remains to be proven.

Atrial Fibrillation↗

Correlation between levels of N-terminal pro-B-type natriuretic peptide and degrees of heart failure.

BACKGROUND: The N-terminal fragment of pro Brain Natriuretic Peptide (NT-pro BNP) is a neuro-hormone synthesized in the cardiac ventricles in response to increased wall tension. The purpose of this study was to assess the correlation between the NT-pro BNP levels and the New York Heart Association function class (NYHA Fc) of dyspnea and echocardiographic findings for the patients who visited our cardiology departments. METHODS: From October, 2002 to April, 2003, serum NT-pro BNP levels were measured in 348 patients who visited the Samsung Medical Center and the Jong Koo Lee Heart Clinic. RESULTS: The NT-pro BNP levels were increased with the progression of NYHA Fc of dyspnea (p < 0.001 by ANOVA), the increase in the systolic left ventricular internal dimension (p < 0.05), and the decrease in the ejection fraction (p < 0.01). For the NYHA Fc I patients, the NT-pro BNP levels were positively correlated with age (0 < 0.001) and left atrial size (p < 0.001). For the patients with ischemic heart disease, the NT-pro BNP levels were also positively correlated with the NYHA Fc (p < 0.001 by ANOVA). The NT-pro BNP levels were increased with the increase in the systolic (p < 0.001) and diastolic pressure (p = 0.017), the left ventricular internal dimension as well as the decrease in the ejection fraction (p < 0.001). The area under the receiver operating characteristic (ROC) curve for the NT-pro BNP levels was 0.994 (95% confidence interval, 0.979-0.999), and the most reliable cut-off level for the NT-pro BNP was 293.6 pg/mL. CONCLUSION: The NT-pro BNP levels were positively correlated with the NYHA Fc of dyspnea and the systolic dysfunction for the patients who visited our cardiology departments. A 300 pg/mL value for the NT-pro BNP cut-off point appears to be a sensitive level to differentiate dyspnea originating from an ailing heart or not for the patients who visited our cardiology departments.

Dyspnea↗

Mitral regurgitation in patients with advanced systolic heart failure.

BACKGROUND: Mitral regurgitation (MR) may develop in patients with advanced systolic congestive heart failure (CHF) without organic mitral valve disease and contribute to worsening symptoms and survival. Surgical mitral annuloplasty improves symptoms in patients with advanced CHF, and percutaneous approaches to mitral annuloplasty are being developed. Our objective was to define the prevalence, clinical correlates, and prognostic implications of functional MR and the use of mitral annuloplasty in patients with advanced systolic CHF evaluated in a heart failure clinic. METHODS AND RESULTS: We reviewed clinical, echocardiographic, and survival data from all patients with advanced systolic CHF (New York Heart Association class III or IV; ejection fraction </=35%) resulting from ischemic or idiopathic cardiomyopathy who were evaluated at our heart failure clinic between January 1996 and September 2001. Of 716 patients with advanced CHF, 558 had satisfactory baseline echocardiograms performed at our institution. Among these patients, MR was severe in 24 (4.3%), moderate-severe in 70 (12.5%), moderate in 122 (21.9%), mild-moderate in 66 (11.8%), mild in 218 (39.1%), and absent or present as only a trace in 58 (10.4%). The severity of MR was confirmed by quantitative analysis in 72% of patients with hemodynamically significant MR (more than moderate). The severity of MR correlated with the severity of systolic dysfunction (P <.001), ventricular dilatation (P <.03), atrial dilatation (P <.001), diastolic dysfunction (P <.001), and pulmonary hypertension (P <.001). Coexistent severe or moderate-severe tricuspid regurgitation was present in 25% of patients with hemodynamically significant MR. Patients with hemodynamically significant MR had higher mortality (P=.03) but not when controlling for age, sex, cause, New York Heart Association class, and ejection fraction (P=.95). Only 3 patients subsequently underwent mitral valve repair. CONCLUSION: Among patients with advanced CHF, hemodynamically significant MR is common. The severity of MR did not provide independent prognostic information in this group recognized to have uniformly high mortality.

Aged↗

Endomyocardial biopsy in hemochromatosis: clinicopathologic correlates in six cases.

Clinical and pathologic features of cardiac hemochromatosis diagnosed by endomyocardial biopsy in six men, aged 32 to 75 years (mean 52), are described. Echocardiography demonstrated left ventricular enlargement and marked global systolic dysfunction in five. Cardiac catheterization demonstrated normal coronary arteries, increased left ventricular end-diastolic pressure and decreased left ventricular systolic function in all five so studied. Stainable iron was present in all endomyocardial biopsy specimens from the five patients with decreased left ventricular systolic function. Histologically, iron was detected only within the sarcoplasm, and its extent varied inversely with ventricular function. Thus, cardiac hemochromatosis represents a storage rather than an infiltrative disease. These results indicate that stainable iron is consistently observed in endomyocardial biopsy specimens from patients with impaired left ventricular systolic function. Iron staining is recommended for endomyocardial biopsy specimens from patients with idiopathic cardiac dysfunction.

Adult↗

Heart rate variability in human immunodeficiency virus-positive individuals.

BACKGROUND: Heart rate variability (HRV) is a marker of cardiac autonomic tone. Depressed HRV has been reported in patients with AIDS. We conducted this study to find out if HRV is depressed in human immunodeficiency virus (HIV)-positive individuals without AIDS. METHODS: We studied prospectively HRV by spectral analysis of short-term electrocardiography (ECG) monitoring in 21 HIV-positives (33+/-11 years) and in 18 healthy volunteers (31+/-9 years). None of the HIV-positives had any clinical evidence of autonomic or cardiac dysfunction. Echocardiography was also performed in HIV-seropositives to rule out left ventricular (LV) systolic dysfunction. All these individuals did not have any evidence of AIDS. RESULTS: Mean CD4+ lymphocyte count was 426+/-166/mm(3). The ejection fraction (EF%) of HIV patients was 62.4+/-6.4. The total power of HRV was reduced significantly in HIV-positive individuals (p<0.00001). All the components of HRV were reduced. CONCLUSIONS: HRV is reduced in HIV-seropositive individuals in early stages of infection as well without any clinical evidence of autonomic dysfunction. This may serve as an early marker of future global sympatho-vagal imbalance.

Adult↗

Compensated volume overload increases the vulnerability of heart mitochondria without affecting their functions in the absence of stress.

Although mitochondrial dysfunction has often been associated to heart failure, it has been suggested that it may represent only a late phenomenon in the disease process. We hypothesized that mitochondrial vulnerability to stress could be impaired in hypertrophied but non-decompensated hearts at a time when overt mitochondrial defects are not yet apparent. In the present study, hypertrophic remodeling was induced by means of an aorto-caval fistula (ACF) in WKHA rats and experiments were performed 12 weeks post surgery. At this time, ACF animals displayed normal contractile function, tissue oxidative capacity as well as mitochondrial membrane potential and respiratory function. However, compared to sham, mitochondria from ACF animals were more vulnerable to anoxia-reoxygenation injury in vitro as indicated by a greater impairment of oxidative phosphorylation and a greater dependence of respiration on exogenous NADH. Addition of the PTP inhibitor CsA restored respiratory function to the level observed in mitochondria from sham animals. Likewise, mitochondria from ACF displayed a greater sensitivity to Ca(2+)-induced PTP opening in vitro compared to their sham counterparts. In addition to the greater vulnerability of mitochondria in vitro, mitochondrial PTP opening measured in situ in perfused hearts was greater following ischemia-reperfusion in ACF animals than in their sham counterparts. This was associated with a more impaired functional recovery and greater tissue damage during reperfusion in hearts from ACF vs sham. Taken together, these results indicate that, in response to volume overload, mitochondria may display increased vulnerability in the absence of any sign of dysfunction under baseline unstressed conditions, at a time when adverse ventricular remodelling is observed but systolic dysfunction and decompensation have not occurred yet.

Animals↗

Myocardial contractility does not determine the haemodynamic response during dialysis.

BACKGROUND: LV systolic dysfunction in dialysis patients has been implicated in the genesis of dialysis hypotension. End-systolic elastance (E(es)), a relatively load-independent parameter of myocardial contractility, was assessed by testing the acute left ventricular (LV) response to nitroglycerine (NTG) in hypotension-prone (HP) and hypotension-resistant (HR) patients. METHODS: Routine measurement of ejection fraction (EF) was done before dialysis in 15 patients without significant valvular disease or symptoms of coronary heart disease. Continuous arterial pressure was measured by Finapres, with systolic blood pressure (SBP) as surrogate for LV end-systolic pressure. Simultaneously, LV area was measured using automated border detection. SBP and LV area data were combined online to create pressure-area loops in real time following intravenous NTG bolus. E(es) was determined offline by beat-to-beat analysis of consecutive pressure-area loops. RESULTS: SBP, at baseline 168 mmHg (128-188 mmHg), decreased to 127 mmHg (79-161 mmHg). End-systolic LV area, at baseline 6 cm2 (1-12 cm2), decreased to 4 cm2 (1-10 cm2). E(es) in the HP group (11 mmHg cm(-2); 7-22 mmHg cm(-2)) was not different from E(es) in the HR group (9 mmHg cm(-2); 4-16 mmHg cm(-2)). EF was 61% (45-73%). There was no correlation between E(es) and EF. CONCLUSIONS: In this population of dialysis patients without clinically manifest heart disease, the HP and HR groups had a similar E(es). Therefore, these two types of dialysis patients were not distinguished by a difference in myocardial contractility. The results of this study argue against a role for reduced myocardial contractility in the genesis of intradialytic hypotension.

Adult↗

[Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction].

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.

Adolescent↗

The impact of the AMPD1 gene polymorphism on exercise capacity, other prognostic parameters, and survival in patients with stable congestive heart failure: a study in 686 consecutive patients.

BACKGROUND: Previous studies have demonstrated that the adenosine monophosphate deaminase 1 (AMPD1) C34T polymorphism may be associated with survival in cardiac populations with a protective effect of the T allele. However, these studies included limited number of patients with few cardiovascular events. METHODS: We prospectively analyzed the impact of the C34T polymorphism of the AMPD1 gene in 686 unrelated white patients with stable congestive heart failure related to left ventricular systolic dysfunction. Patients underwent echocardiography, radionuclide angiography, and a cardiopulmonary exercise test. Blood samples were drawn for standard and hormonal determinations and for genetic analysis. RESULTS: There were 517 (75%) CC homozygotes, 155 (23%) CT heterozygotes, and 14 (2%) TT mutated homozygotes. We did not demonstrate any impact of this polymorphism on clinical, biologic, echocardiographic, radionuclide, and exercise parameters in the whole population and in ischemic and nonischemic subgroups of patients. During a median follow-up period of 3 years, there were 145 cardiac-related deaths and 6 urgent transplantations. There was no impact of this polymorphism on survival. CONCLUSIONS: In our population, we did not demonstrate any effect of the C34T polymorphism of the AMPD1 gene on major congestive heart failure parameters and on survival.

AMP Deaminase↗

Echocardiographic characterization of fundamental mechanisms of abnormal diastolic filling in diabetic rats with a parameterized diastolic filling formalism.

Abnormalities of diastolic function (DF) precede systolic dysfunction in diabetic cardiomyopathy. Transmitral Doppler flow analysis is the primary method for noninvasively assessing DF. We used model-based Doppler E-wave analysis to evaluate diastolic function differences between normal and diabetic rat hearts. Control rats and those with diabetes underwent echocardiography with analysis by traditional Doppler indexes and by the parameterized diastolic filling (PDF) formalism, generating 3 parameters, x0, c, and k, that uniquely characterize each E-wave. Significant intergroup differences in the E/A ratios (P <.01), isovolumic relaxation times (P <.01), and the modeling parameter c (P <.05) were found. There were no significant differences in shortening fraction, deceleration time, myocardial collagen content, or the parameters x0 and k between diabetic and control rats. These results indicate that differences in diastolic function may be noninvasively quantified and that diabetic hearts may exhibit defects in uncoupling of the contractile apparatus without concomitant increases in chamber stiffness.

Animals↗

Poor relationship between exercise capacity and spirometric measurements in patients with more symptomatic heart failure.

BACKGROUND: The origin of exercise limitation in patients with chronic heart failure (CHF) is multifactorial, and the relative contributions of different abnormalities may vary with severity of heart failure symptoms. The aim of the current study was to determine the extent to which spirometric indices predict peak exercise capacity in patients with differing severity of symptoms. METHODS AND RESULTS: A total of 340 patients with left ventricular systolic dysfunction underwent spirometry, and a ramped, maximal exercise treadmill test with metabolic gas exchange measurements. For comparative purposes, a group of 174 aged-matched controls with no major structural heart disease (MSHD) was also included. In a stepwise linear regression model, forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) were independent predictors of peak oxygen uptake (pVO2) in controls (r2= 18-25%; P = .001) and New York Heart Association (NYHA) I-II patients (r2= 16-18%; P = .001). No association between spirometric indices (FEV1/FVC) and pVO2 (r2= 1-2%; P > .05) was found in NYHA III-IV patients. CONCLUSION: In aged-matched controls with no MSHD, spirometric variables (FEV1/FVC) explain 18% to 25% of the variance in pVO2, and 16% to 18% of the variance in patients with NYHA class I-II symptoms. As symptoms worsen, the influence of spirometric variables on peak exercise capacity diminishes, and there is no such relation in the NYHA class III-IV patients.

Aged↗