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PubMed2001

Echocardiographic evaluation of right ventricular systolic functions in pure mitral stenosis.

Detailed echocardiographic evaluation of right ventricular muscle thickness and systolic functions was performed in twenty two cases of isolated rheumatic mitral stenosis without clinical signs of systemic venous congestion, tricuspid regurgitation or atrial fibrillation. Twenty two age and sex matched normal persons formed the control group. Right ventricular thickness was significantly increased in the patients with mitral stenosis. End-diastolic and end-systolic long axis measurements and areas were significantly increased and fractional shortening of these parameters was significantly reduced in the patient group. Our results show that right ventricular systolic functions are significantly impaired even in absence of clinical signs of systemic venous congestion. This impairment of systolic function did not correlate with pulmonary flow acceleration time. Myocardial involvement in rheumatic process could be one possibility. Systolic movement of the Tricuspid annulus and right ventricular mid cavity short axis dimension were not sensitive in detecting right ventricular systolic dysfunction.

Female↗
PubMed1998

Monocyte chemoattractant protein 1 (MCP-1) gene expression in dilated cardiomyopathy.

The cytotoxic action of leukocytes may be a most probable cause of cardiac myocyte damage seen in chronic myocarditis and dilated cardiomyopathy (DCM). The migration and tissue infiltration of leukocytes is regulated by chemotactic cytokines. Recently, the presence of monocyte chemoattractant protein 1 (MCP-1) messenger RNA has been demonstrated in endomyocardial biopsy tissue obtained from patients with DCM. This chemokine could contribute to enhanced leukocyte recruitment and activation resulting in chronic damage of cardiomyocytes. Accordingly, we sought to determine whether the severity of left ventricular dysfunction in DCM is associated with quantitative alterations of MCP-1 messenger RNA and MCP-1 protein in endomyocardial biopsy tissue. A group of DCM patients with low to moderate impairment of left ventricular function (ejection fraction 45.3+/-2.3%, n=7) was compared to patients with severe left ventricular dysfunction (ejection fraction 25.5+/-3.1%, n=7). MCP-1 messenger RNA expression was determined by quantitative polymerase chain reaction. MCP-1 protein and the presence of infiltrating inflammatory cells were detected by immunohistochemistry. DCM patients with severe left ventricular dysfunction showed a 2.35 fold higher MCP-1 messenger RNA expression when compared to DCM patients with less severe dysfunction (P=0.0229). Positive immunohistochemical staining for MCP-1 was found in all seven patients with severe left ventricular dysfunction and was particularly distinct within the cardiac interstitum. In five of seven patients with less severe systolic dysfunction, MCP-1 protein was found, but was less pronounced and distributed in patchy interstitial areas, close to intramyocardial vessels. Furthermore, there was a consistent trend toward a higher infiltration of inflammatory cells in DCM patients with lower ejection fraction. In conclusion, MCP-1 is dynamically regulated in DCM related deterioration of left ventricular function. This mechanism might contribute to myocyte damage via infiltrated and activated monocytes.

Adult↗
PubMed1993

Differentiating systolic from diastolic heart failure: pathophysiologic and therapeutic considerations.

PURPOSE: To compare and contrast the pathophysiology and therapy of heart failure with normal and abnormal systolic ventricular function. METHODS: Review of basic pathophysiologic mechanisms, clinical data, and therapeutic trials. CONCLUSIONS: The clinical features of heart failure may be similar regardless of whether ventricular function is normal or abnormal. However, the pathophysiologic mechanisms leading to heart failure with normal ventricular function differ considerably from those producing heart failure with abnormal systolic function. The key problems in heart failure with abnormal systolic function involve impaired contractility, neuroendocrine activation, increased intracardiac volume and pressure, and enhanced sensitivity to change in afterload. With normal systolic function, the key problem is an abnormal diastolic pressure/volume relationship, which may be due to a variety of active and passive processes affecting diastole. Assessing left ventricular systolic function is crucial before initiating therapy in a patient with heart failure, since treatment for systolic dysfunction may be ineffective or even counterproductive if symptoms are due to abnormal diastolic properties with preserved systolic function.

Clinical Trials as Topic↗
PubMed2006

Evaluation of eplerenone in the subgroup of EPHESUS patients with baseline left ventricular ejection fraction <or=30%.

AIMS: Because of the prognostic importance of LV dysfunction following an AMI and the increasing use of electrical and/or mechanical interventions in patients with LV systolic dysfunction, this retrospective analysis of EPHESUS patients with LVEF <or=30% at baseline was conducted to determine the value of eplerenone in this setting. METHODS AND RESULTS: In EPHESUS, 6,632 patients with LVEF <or=40% and clinical heart failure (HF) post-AMI who were receiving standard therapy were randomized to eplerenone 25 mg/day titrated to 50 mg/day or placebo for a mean follow-up of 16 months. Treatment with eplerenone in the subgroup of patients with LVEF <or=30% (N=2106) resulted in relative risk reductions of 21% versus placebo in both all-cause mortality (P=0.012) and cardiovascular (CV) mortality/CV hospitalization (P=0.001), and 23% for CV mortality (P=0.008). The relative risk of sudden cardiac death (SCD) was reduced 33% (P=0.01) and HF mortality/HF hospitalization was reduced 25% (P=0.005) with eplerenone compared with placebo. Within 30 days of randomization, eplerenone resulted in relative risk reductions of 43% for all-cause mortality (P=0.002), 29% for CV mortality/CV hospitalization (P=0.006), and 58% for SCD (P=0.008). CONCLUSIONS: Treatment with eplerenone plus standard therapy in patients with post-AMI HF and LVEF <or=30% provided significant incremental benefits in reducing both early and late mortality and morbidity.

Adult↗
PubMed2003

Reversible myocardial dysfunction, a possible complication in critically ill patients without heart disease.

PURPOSE: Reversible myocardial dysfunction or myocardial stunning is frequently described in patients with episodes of acute coronary syndrome and has recently been reported in critically ill patients without ischaemic heart disease. This article presents a study and description of the possible existence of myocardial dysfunction in critically ill patients in our setting who present no acute episode or history of cardiovascular disease. DESIGN: Prospective, descriptive study. SETTING: The intensive care unit of a district hospital. PATIENTS AND PARTICIPANTS: The study included all patients admitted to the intensive care unit between March 1998 and March 2001 for noncardiac causes and with no history of heart disease, and who underwent echocardiographic examination for electrocardiographic changes, signs of cardiac insufficiency, persistent arrhythmias, or any other indication. Patients with sepsis or other critical illness known to be associated with myocardial dysfunction were excluded from the study. The study was carried out on those selected patients who developed myocardial dysfunction. MEASUREMENTS AND RESULTS: Transthoracic and transoesophageal echocardiography were carried out to assess the left ventricular ejection fraction and any segmental contractility disturbances. These investigations were carried out within 24 hours of admission, during the first week, during the second or third week, after one month and after three to 6 months. The electrocardiogram was assessed on admission and the changes over time were studied. Thirty-three patients were included in the study after detecting myocardial dysfunction; the median age of these patients was 63 years [range, 23-82 years]. Seven patients died. The median initial left ventricular ejection fraction was 0.34 [range, 0.16-0.48] and improved with time. Segmental contractility disturbances were detected initially in all patients and also normalized with time. All patients presented electrocardiogram changes that normalised in line with the echocardiographic changes. CONCLUSIONS: Reversible myocardial dysfunction can be develop in critically ill patients without primary heart disease. This syndrome is associated with systolic dysfunction, segmental contractility disturbances and electrocardiographic changes.

APACHE↗
PubMed2002

Evidence for an active inflammatory process in the hibernating human myocardium.

Myocardial hibernation refers to a state of prolonged impairment of left ventricular function in the presence of coronary artery disease, which may be reversed by revascularization. In this study we present evidence for a local inflammatory reaction in hibernating myocardial segments from patients undergoing coronary revascularization. We obtained transmural myocardial biopsies guided by transesophageal echocardiography from patients with ischemic ventricular dysfunction undergoing bypass surgery. Among the 28 biopsied segments included in the study, 23 showed evidence of systolic dysfunction. The majority of dysfunctional segments (85.7%) were viable ((201)Tl uptake >/= 60%). The samples were stained with markers for mast cells, mature resident macrophages, and the monoclonal antibody Mac387 that labels newly recruited myeloid cells. Dysfunctional segments showed more extensive fibrosis and higher macrophage density than normal segments. Among the 23 dysfunctional segments, 12 recovered function as assessed with echocardiograms 3 months after revascularization. Segments with postoperative functional recovery had comparable macrophage and mast cell density with those showing persistent dysfunction. However, biopsied segments that subsequently recovered function contained significantly higher numbers of newly recruited Mac387-positive leukocytes (18.7 +/- 3.1 cells/mm(2), n = 12 versus 8.6 +/- 0.9 cells/mm(2), n = 11; P = 0.009). In addition, monocyte chemotactic protein-1, a potent mononuclear cell chemoattractant, was predominantly expressed in segments with recovery of function. Myocardial hibernation is associated with an inflammatory response leading to active leukocyte recruitment. Dysfunctional myocardial segments that show an active inflammatory reaction have a greater potential for recovery of function after revascularization. We postulate that revascularization may promote resolution of the ongoing inflammation, preventing further tissue injury and fibrosis.

Aged↗
PubMed1994

Impaired cardiac function in rats with healed myocardial infarction: cellular vs. myocardial mechanisms.

The inotropic responsiveness of isolated perfused rat hearts and single left ventricular (LV) myocytes to extracellular Ca2+ ([Ca2+]o) was examined 3 wk after ligation of left main coronary artery. Myocytes isolated from myocardial infarcted (MI) hearts were 10% longer. At [Ca2+]o of 1.1 mM, cell shortening as well as intracellular Ca2+ concentration dynamics were similar between MI and sham LV myocytes. At [Ca2+]o of 4.9 mM, maximal extent of cell shortening was significantly less in MI myocytes (16 +/- 1 vs. 22 +/- 1%), and peak intracellular Ca2+ concentration was also substantially lower. Thus, under conditions of high [Ca2+]o, decreased sarcolemmal Ca2+ influx and Ca2+ release during excitation-contraction may contribute to systolic dysfunction in MI hearts. Perfused working hearts and isovolumic heart preparations with infarcted LV displayed depressed maximal systolic pressure and decreased sensitivity to the inotropic effects of [Ca2+]o. Our data also indicate that, in addition to possible abnormalities in the contractile response of single myocytes, global factors such as loss of functional myocardium, altered chamber geometry, tissue fibrosis, and/or subendocardial ischemia contributed to depressed LV function in post-MI hearts perfused at physiological [Ca2+]o.

Animals↗
PubMed1997

Physical and physiological determinants of pulmonary venous flow: numerical analysis.

To study the physical and physiological determinants of transmitral and pulmonary venous flow, a lumped-parameter model of the cardiovascular system has been created, modeling the instantaneous pressure, volume, and influx/efflux of the pulmonary veins, left atrium and ventricle, systemic arteries and veins. right atrium and ventricle, and pulmonary arteries. Initial validation has been obtained by direct comparison with transesophageal echocardiographic recordings of mitral and pulmonary venous velocity for the following clinical situations: normal diastolic function, delayed ventricular relaxation, restrictive filling due to severe systolic dysfunction, severe mitral regurgitation before and after valve repair surgery, and premature atrial contraction occurring during ventricular systole. Sensitivity analysis has been performed with a Jacobian matrix, representing the proportional change in a group of output indexes (yi) in response to isolated changes in input parameters (xj), [(delta yi/yi)/ ([delta xj/xj)], demonstrating the complementary nature of mitral and pulmonary venous A-wave velocity for predicting ventricular stiffness and atrial systolic function. This unified numerical-experimental programming environment should facilitate model refinement and physiological data exploration, in particular guiding more accurate interpretations of Doppler echocardiographic data.

Animals↗
PubMed1996

Tumor necrosis factor-alpha induces a biphasic effect on myocardial contractility in conscious dogs.

Tumor necrosis factor-alpha (TNF-alpha) likely plays a role in the pathophysiology of myocardial depression observed in septic shock. To evaluate the hemodynamic effects of TNF-alpha in vivo while eliminating the influence of altered sympathetic tone, eight conscious chronically instrumented dogs were studied after pretreatment with propranolol (2 mg/kg) and atropine (2mg). Using three sets of piezoelectric crystals to measure left ventricular (LV) volume and LV manometers to measure pressure, we determined load-independent parameters of LV systolic performance before, during, and after infusion of recombinant human TNF-alpha (rhTNF-alpha, 40 micrograms/kg for 1 hour). Plasma was analyze for epinephrine and norepinephrine. Between 1 and 7 hours of exposure, rhTNF-alpha induced significant increases in circulating catecholamines. Norepinephrine rose from 268.6 +/- 47.2 to 426.2 +/- 87.0 pg/mL (P < .05) at 1 hour and peaked at 921.2 +/- 156.8 pg/mL (P < .001) at 4 hours after initiating rhTNF-alpha treatment. Similarly, epinephrine increased from 130.2 +/- 30.9 to 884.5 +/- 210.2 pg/mL (P < .05) at 1 hour and peaked at 3195.3 +/- 476 pg/mL (P < .001) at 4 hours. Before the surge of circulating catecholamines and despite complete beta adrenergic blockade, rhTNF-alpha induced a 7% to 40% increase in LV contractile performance during the 60-minute infusion. After this initial positive inotropic effect, rhTNF-alpha treatment led to precipitous systolic dysfunction between 2 and 7 hours of exposure; this myocardial depressant effect persisted at 25 hours. LV systolic performance declined to 19% to 35% of baseline values, depending on the specific contractile parameter evaluated. We conclude that rhTNF-alpha affects LV systolic function in a time-dependent biphasic manner. Increases in circulating catecholamines after rhTNF-alpha infusion cannot account for the early improvement in LV systolic performance.

Animals↗
PubMed1995

Left ventricular geometry and cardiac function in mild to moderate essential hypertension.

To elucidate left ventricular (LV) cardiac structure and function in patients with mild to moderate essential hypertension, we studied the relationship between LV geometry and function. We evaluated LV diastolic and systolic functions by M-mode echocardiography in 91 age-matched normotensive control subjects (NT) and 124 patients with essential hypertension. Hypertensive patients were divided into two groups based on the WHO stage classification: WHO I (n = 76) and WHO II (n = 48). Patients in WHO I and WHO II were further categorized according to the relative wall thickness as normal left ventricle (n = 47), concentric remodeling (n = 29), concentric hypertrophy (n = 25), and eccentric hypertrophy (n = 23). LV diastolic function was significantly decreased in the hypertensive groups compared to NT. There was no significant difference in LV systolic performance among NT, WHO I and WHO II. LV contractility was significantly increased in WHO I compared to NT. In respect to ventricular geometric pattern, LV diastolic function was significantly decreased in both the concentric hypertrophy and eccentric hypertrophy groups. LV systolic dysfunction was noted only in the eccentric hypertrophy group. In conclusion, patients with concentric remodeling had normal systolic and diastolic functions. LV diastolic function was impaired in both the concentric and eccentric hypertrophy groups due to an increase in LVMi. Moreover, LV systolic impairment was noted in the eccentric hypertrophy group due to an inappropriate compensation to LV systolic load.

Adult↗
PubMed2004

[Brain natriuretic peptide].

Plasma levels of various neurohumoral factors are activated and have an important role of the pathophysiology of congestive heart failure (CHF). Atrial natriuretic peptide (ANP) and brain (or B-type) natriuretic peptide (BNP) are secreted from cardiomyocytes in response to atrial or ventricular wall stretch. The natriuretic peptides have a fundamental role in cardiovascular remodeling, volume homeostasis, and the response to myocardial injury. Clinical investigations of these peptides have focused on their diagnostic usefulness for heart failure and left ventricular dysfunction and their prognostic usefulness after acute coronary syndromes and heart failure. In patients with left ventricular systolic dysfunction, a high plasma BNP level is an independent prognostic predictor of CHF patients, suggesting that the compensatory activity of the cardiac natriuretic peptide system is attenuated as mortality increases in chronic CHF patients with high plasma levels of ANP and BNP. BNP is more useful than ANP for diagnosis and management of CHF. Recently, rapid BNP assay is available in our country, rapid measurement of BNP in the emergency department may improve the evaluation and treatment of patients with acute dyspnea and thereby reduced the time to discharge and the total cost of treatment. In addition, BNP-guided treatment of heart failure may reduce total cardiovascular events, and delayed time to first event combination with intensive clinically guided treatment.

Biomarkers↗
PubMedDate not supplied

Importance of early diagnosis and therapy of acute meningococcal myocarditis: a case report with review of literature.

Acute meningococcemia is a clinical syndrome resulting from Neisseria meningitides infection. The clinical presentation is varied, but when associated with myocardial dysfunction, it carries a poor prognosis. We report a case of meningococcal myocarditis causing severe left ventricular systolic dysfunction that improved over a 4-day period after appropriate antimicrobial treatment following prompt diagnosis. The case highlights the importance of prompt recognition and treatment of this disorder.

Adolescent↗
PubMed2000

A case of arrhythmogenic right ventricular cardiomyopathy in sinus rhythm associated with thrombus in the right atrium.

We describe a patient with arrhythmogenic right ventricular cardiomyopathy (ARCV) in sinus rhythm associated with thrombus in the right atrium. The occurrence of a right heart thrombus in ARCV is extremely rare and, to our knowledge, has been previously reported only in the right ventricle. In our case, ARCV most probably led to right atrial spontaneous echo contrast, and later, right atrial thrombus formation by blood stasis caused by right ventricular systolic dysfunction. In conclusion, our case suggests that right atrial thrombus may occur in ARCV, even in sinus rhythm.

Adult↗
PubMed2003

Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both.

BACKGROUND: Angiotensin-converting-enzyme (ACE) inhibitors such as captopril reduce mortality and cardiovascular morbidity among patients with myocardial infarction complicated by left ventricular systolic dysfunction, heart failure, or both. In a double-blind trial, we compared the effect of the angiotensin-receptor blocker valsartan, the ACE inhibitor captopril, and the combination of the two on mortality in this population of patients. METHODS: Patients receiving conventional therapy were randomly assigned, 0.5 to 10 days after acute myocardial infarction, to additional therapy with valsartan (4909 patients), valsartan plus captopril (4885 patients), or captopril (4909 patients). The primary end point was death from any cause. RESULTS: During a median follow-up of 24.7 months, 979 patients in the valsartan group died, as did 941 patients in the valsartan-and-captopril group and 958 patients in the captopril group (hazard ratio in the valsartan group as compared with the captopril group, 1.00; 97.5 percent confidence interval, 0.90 to 1.11; P=0.98; hazard ratio in the valsartan-and-captopril group as compared with the captopril group, 0.98; 97.5 percent confidence interval, 0.89 to 1.09; P=0.73). The upper limit of the one-sided 97.5 percent confidence interval for the comparison of the valsartan group with the captopril group was within the prespecified margin for noninferiority with regard to mortality (P=0.004) and with regard to the composite end point of fatal and nonfatal cardiovascular events (P<0.001). The valsartan-and-captopril group had the most drug-related adverse events. With monotherapy, hypotension and renal dysfunction were more common in the valsartan group, and cough, rash, and taste disturbance were more common in the captopril group. CONCLUSIONS: Valsartan is as effective as captopril in patients who are at high risk for cardiovascular events after myocardial infarction. Combining valsartan with captopril increased the rate of adverse events without improving survival.

Aged↗
PubMed1990

Determinants of hemodynamic compromise with severe right ventricular infarction.

To elucidate determinants of hemodynamic compromise in patients with acute right ventricular (RV) infarction, we studied 16 patients with hemodynamically severe RV infarction by right heart catheterization and two-dimensional ultrasound. Severe RV systolic dysfunction, evident by ultrasound in all patients as RV dilatation and depressed RV free wall motion, was associated with a broad sluggish RV waveform, diminished peak RV systolic pressure (27.6 +/- 4.5 mm Hg), and depressed RV stroke work (4.6 +/- 2.4 g.m/m2). Paradoxical septal motion was consistently noted. In some cases, the septum bulged into the right ventricle in a pistonlike fashion and appeared to mediate systolic ventricular interaction through which left ventricular septal contraction contributed to RV pressure generation. RV diastolic dysfunction was indicated by elevated RV end-diastolic pressures (13.7 +/- 2.7 mm Hg), RV "dip and plateau," equalization of diastolic filling pressures, and reversal of diastolic septal curvature toward the volume-deprived left ventricle. A prominent right atrial (RA) X and blunted Y descent, indicative of impairment of RV filling throughout diastole, were confirmed in all patients by their relation to RV systolic events. Patients manifested one of two distinct RA waveform morphologies differentiated by A wave amplitude and associated with disparate clinical courses. In eight patients, an RA W pattern was evident, characterized by augmented A waves; eight others manifested an M pattern constituted by depressed A waves. Compared with those with an M pattern, patients with a W pattern had higher peak RV pressures (29.6 +/- 3.8 versus 25.5 +/- 4.3 mm Hg, p less than 0.05), better cardiac output (3.4 +/- 0.3 versus 2.9 +/- 0.7 l/min, p less than 0.05), more favorable response to volume and inotropes, and less frequently required emergency revascularization for refractory shock (none versus five for those with an M pattern). Patients with a W pattern were more severely compromised if atrioventricular dyssynchrony developed and were more dramatically improved by restoration of physiological rhythm. Angiography in patients with depressed A waves demonstrated more proximal coronary obstruction leading to ischemic compromise of RA function, whereas in those with augmented A waves, the culprit lesion was proximal to the RV but distal to the RA branches. These results indicate that hemodynamic compromise in patients with RV infarction is exacerbated by decreased preload reserve that is dependent on atrial systole. The amplitude of the RA A wave, an indication of the status of RA function, is an important determinant of RV performance and hemodynamic compromise.

Blood Pressure↗
PubMed1995

Valve replacement for regurgitant lesions of the aortic or mitral valve in advanced left ventricular dysfunction.

Patients with aortic regurgitation and severe left ventricular dysfunction remain candidates for aortic valve replacement, as long as the risks of late left ventricular dysfunction and congestive heart failure have been fully discussed with the patient, the patient's family, and the referring physician. In contrast, patients with mitral regurgitation and severe systolic dysfunction are at considerable risk of more severe left ventricular dysfunction after operation, especially if mitral valve repair or chordal-sparing procedure cannot be performed. In patients who are candidates for such procedures that preserve the integrity of the subvalvular mitral apparatus, operation may be successful in selected patients despite moderate-to-severe depression of systolic function. Prognosis is guarded to poor in patients with regurgitant valvular lesions and advanced left ventricular dysfunction, and the emerging alternative treatments discussed in other articles in this Cardiology Clinics deserve consideration in these patients.

Aortic Valve↗
PubMedDate not supplied

[The types of the structural-functional connections of the coronary circulation and the state of the myocardium in patients with isolated and combined forms of ischemic heart disease and arterial hypertension].

The analysis of evidence obtained at coronaroangiography, myocardial scintigraphy, echocardiography, severity of coronary and heart insufficiency in patients with isolated and combined forms of ischemic heart disease and arterial hypertension has identified three types of structural-functional relations between characteristics of coronary circulation and myocardial status: myocardio-perfusional (concentric myocardial hypertrophy with diastolic dysfunction leading to perfusional defects), coronaro-myocardial (affection of coronary arteries resulting in myocardial lesion with primarily systolic dysfunction), coronaro-perfusional (disturbed coronary circulation in involvement of coronary and myocardial factors).

Angiography, Digital Subtraction↗
PubMed1989

Pathophysiology of the failing heart.

Cardiac (or myocardial) failure of acute onset or of chronic duration is the result of a structural and/or biochemical remodeling of the myocardium. This, in turn, compromises the contractile performance of the myocardium. The hypertrophic growth of myocytes and the architectural transformation of ventricular chamber size and shape--while initially useful compensatory responses--do not prevent the inevitable appearance of pump failure where oxygen delivery to the metabolizing tissues becomes inadequate. Indeed, the severity of cardiac failure can be judged from the level of oxygen consumption that elicits this state of impaired oxygen supply and demand. A better understanding of the mechanical behavior of the ventricular chamber, including its elastic and resistive properties, together with recent advances in our ability to measure instantaneous ventricular pressure and volume, may prove useful in identifying pathologic features of hypertrophy and dilatation in individual patients. In grading the severity of failure and comparing groups of patients, a normalization of the mechanical parameters by differences in chamber size, shape, and mass is necessary. Symptomatic cardiac failure, based invariably on inadequate oxygen delivery and/or pulmonary congestion, is more commonly the result of ventricular systolic dysfunction. Abnormalities in diastolic function, including ventricular relaxation and filling, while less common and often associated with preserved systolic pump function, do occur. Finally, it must be recognized that the failing ventricle carries an additional hydraulic load that arises from the arterial circulation to which it is coupled.(ABSTRACT TRUNCATED AT 250 WORDS)

Forced Expiratory Flow Rates↗