Atrial septal defect: attenuation of respiratory variation in systolic and diastolic time intervals.

The effects of pathologic states on right and left ventricular function have been studied extensively. However, there have been few studies on the interrelations between right and left ventricular function in normal human subjects and in patients with disease. Respiratory effects on ventricular interrelations reflected by diastolic time, right or left ventricular systolic time and ventricular performance (pre-ejection period/ejection time ratio) were studied in 12 normal subjects and 15 patients with a normal pressure-large shunt atrial septal defect. Simultaneous pulmonary artery (intracardiac manometer recordings) and left ventricular external recordings were performed in both groups. Left ventricular diastolic time increased with inspiration in the normal subjects and decreased in the patients with atrial septal defect (12.6 +/- 2.39 [1 SE] versus -13.4 +/- 3.48 ms, p less than 0.001). Left ventricular systolic time and ejection time decreased with inspiration in the normal group and remained unchanged in the patient group (-7.6 +/- 0.95 versus -0.9 +/- 0.77 ms, p less than 0.001 and -10.4 +/- 1.09 versus -1.7 +/- 0.80 ms, p less than 0.001, respectively). Left ventricular pre-ejection period/ejection time ratio increased with inspiration in the normal subjects and remained unchanged in the patients with atrial septal defect (0.03 +/- 0.008 versus 0 +/- 0.01, p less than 0.01). Right ventricular diastolic time decreased with inspiration in normal and patient groups (-8.8 +/- 1.6 versus -17 +/- 3.87 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

The Marfan syndrome: abnormal aortic elastic properties.

Aortic distensibility and aortic stiffness index were measured at the ascending aorta (3 cm above the aortic valve) and the mid-portion of the abdominal aorta from the changes in echocardiographic diameters and pulse pressure in 14 patients with the Marfan syndrome and 15 age- and gender-matched normal control subjects. The following formulas were used: 1) Aortic distensibility = 2(Changes in aortic diameter)/(Diastolic aortic diameter) (Pulse pressure); and 2) Aortic stiffness index = ln(Systolic blood pressure)/(Diastolic blood pressure)(Changes in aortic diameter)/Diastolic aortic diameter. Pulse wave velocity was also measured. Compared with normal subjects, patients with the Marfan syndrome had decreased aortic distensibility in the ascending and the abdominal aorta (2.9 +/- 1.3 vs. 5.6 +/- 1.4 cm2 dynes-1, p less than 0.001 and 4.5 +/- 2.1, vs. 7.7 +/- 2.5, cm2 dynes-1, p less than 0.001, respectively) and had an increased aortic stiffness index in the ascending and the abdominal aorta (10.9 +/- 5.6 vs. 5.9 +/- 2.2, p less than 0.005 and 7.1 +/- 3.1 vs. 3.9 +/- 1.2, p less than 0.005, respectively). Aortic diameters in the ascending aorta were larger in these patients than in normal subjects, but those in the abdominal aorta were similar in the two groups. Linear correlations for both aortic distensibility and stiffness index were found between the ascending and the abdominal aorta (r = 0.85 and 0.71, respectively). Pulse wave velocity was more rapid in the patients than in the normal subjects (11.6 +/- 2.5 vs. 9.5 +/- 1.4 m/s, respectively, p less than 0.01). Thus, aortic elastic properties are abnormal in patients with the Marfan syndrome irrespective of the aortic diameter, which suggests an intrinsic abnormality of the aortic arterial wall.

Postural exercise abnormalities in symptomatic patients with mitral valve prolapse.

The hemodynamics of the supine and upright exercise response in 16 symptomatic women with mitral valve prolapse (Group I) was compared with that in 8 asymptomatic normal control women (Group II). All subjects had supine and upright echocardiography and phonocardiography at rest and none demonstrated mitral regurgitation. All participants then underwent same day graded bicycle exercise, with simultaneous radionuclide angiography in both the upright and the supine posture. Catecholamines were measured, and a variety of volumetric and hemodynamic data were obtained. Group I (patients with mitral valve prolapse) demonstrated a reduced exercise tolerance, especially during upright exercise, as measured by both total exercise duration and maximal work load achieved. Mean total catecholamine measurements were similar between the two study groups at comparable mean heart rate, mean blood pressure and mean rate-pressure (double) product. No difference was observed in the ratio of right to left ventricular stroke counts at rest or during exercise regardless of posture, suggesting that exercise-induced mitral regurgitation did not occur. A difference was noted, however, in left ventricular end-diastolic volume index. At rest, Group I patients exhibited a 42% decrease in this index when sitting upright, and this difference from supine values persisted at submaximal (300 kpm/min) and peak work loads (34 and 29% difference, respectively). This contrasted with the control subjects whose upright end-diastolic volumes at rest, at 300 kpm/min and at peak exercise were reduced 21, 10 and 3%, respectively, compared with supine values. Cardiac index measurements reflected the reduced left ventricular end-diastolic volume observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular disease of connective tissue origin.

Inherited abnormalities of connective tissue elements often cause changes in the structure and function of the cardiovascular system. Well-known heritable disorders of connective tissue in which cardiovascular abnormalities are prominent include the Marfan syndrome and the Ehlers-Danlos syndrome. Connective tissue abnormalities also occur without the associated features of a recognized syndrome. These include isolated valvular prolapse and anuloaortic ectasia. In this review, the cardiovascular features of connective tissue abnormalities--both the recognized syndromes and the isolated abnormalities--are described, important concepts in the diagnosis and treatment of these disorders are reviewed, and the classification of inherited connective tissue abnormalities of the cardiovascular system is discussed.

Morphologic and functional characteristics of the heart in Friedreich's ataxia.

The purpose of this study was to characterize the heart in patients with Friedreich's ataxia by two-dimensional echocardiography, systolic time intervals, and heart biopsy. Ten patients with Friedreich's ataxia (seven females and three males, age 15 +/- 7 years) were compared with 10 age-matched normal subjects (five males and five females, age 16 +/- 7 years). The mean systolic blood pressure in the patients with Friedreich's ataxia was lower (114 +/- 9 mm Hg) than that in the control subjects (122 +/- 8 mm Hg; p less than 0.05); diastolic blood pressures were the same. The heart rate in the patients with Friedreich's ataxia (102 +/- 17 beats/minute) was greater than that in the control subjects (76 +/- 12 beats/minute; p less than 0.001). The interventricular septal wall thickness was much greater in Friedreich's ataxia (13 +/- 2 versus 8 +/- 1 mm, p less than 0.001) as was the posterior wall thickness (13 +/- 3 versus 8 +/- 1 mm, p less than 0.001). The left ventricular end-diastolic diameter was smaller in Friedreich's ataxia (35 +/- 6 mm versus 47 +/- 6 mm; p less than 0.01), and the fractional change of the left ventricular minor axis with systole was greater in Friedreich's ataxia (40 +/- 9 percent versus 33 +/- 5 percent; p less than 0.05). An 11th patient with Friedreich's ataxia (age 33) had clinical heart failure, but his course was complicated by alcohol abuse. Heart biopsy in three patients with Friedreich's ataxia demonstrated myocyte hypertrophy (21.5 +/- 2.0 microns diameter; normal, 14 to 17 microns) and increased fibrosis (16 +/- 9 percent; normal, less than 5 percent). Thus, heart disease in Friedreich's ataxia is characterized by myocyte hypertrophy, interstitial fibrosis, increased left ventricular wall thickness, decreased left ventricular cavity size, sinus tachycardia, and normal systolic function. Further biochemical analysis of tissues may lead to the link of the neurologic and cardiac diseases and eventually to more effective therapy of this condition.

Altered collagen composition in a prolapsing mitral valve with ruptured chordae tendineae.

A patient presented with mitral valve prolapse, ruptured chordae tendineae, severe mitral regurgitation and congestive heart failure. Pathologic studies demonstrated myxomatous changes of both mitral leaflets. Collagen analysis of the valve and of the chordae tendineae revealed the presence of type I collagen in normal quantities and a striking absence of type III and AB collagens. The altered collagen in this patient's mitral valve probably contributed to the development of his mitral valve disorder.

Tricuspid stenosis. Atrial systolic murmur, tricuspid opening snap, and right atrial pressure pulse.

Observations on the atrial systolic murmur, the tricuspid opening snap, and the right atrial pressure pulse of tricuspid stenosis are presented, based on catheter manometer intracardiac sound and pressure recordings in five patients with hemodynamically significant tricuspid stenosis. The manometer-recorded right atrial pressure pulse of tricuspid stenosis differed from the normal, with (1) elevation of right atrial pressure, (2) different morphologic features (tall, spiky A wave complete before C; small V wave with an interruption, the tricuspid opening snap notch at termination of the gradual Y descent; a diastolic plateau, the relatively flat diastolic segment of the right atrial pressure pulse following the tricuspid opening snap notch prior to the next A wave), and (3) the relative lack of right atrial pressure and right atrial pressure pulse response with normal respiration. The atrial systolic murmur, recorded in the right ventricular inflow tract, was complete by S1; the crescendo-decrescendo atrial systolic murmur configuration paralleled the right ventricular-right atrial diastolic pressure gradient at the time of the atrial A wave. The right atrial contraction-relaxation process, as reflected by the right atrial A wave ascent and descent, was complete at the onset of ventricular systole with P-R intervals of 170 to 200 msec. Thus, the timing and configuration of the atrial systolic murmur reflected the timing and completion of the right atrial contraction-relaxation process prior to the onset of right ventricular systole and the configuration of the tricuspid diastolic pressure gradient. The tricuspid opening snap was recorded in the right ventricular inflow tract and occurred at the time of a notch at the termination of the Y descent of the right atrial pressure pulse V wave, while right atrial pressure exceeded right ventricular pressure. The sound-pressure events were consistent with angiographic and echocardiographic studies, which showed doming or ballooning of the mobile, fused, stenotic tricuspid valve into the right ventricle during the Y descent of the right atrial pressure pulse. The tricuspid opening snap occurred at the time of the termination of the diastolic movement of the fused tricuspid unit into the right ventricle. These observations are presented within the framework of previous studies in order to trace the development of medical ideas about the pathophysiologic basis for the sound and pressure events of tricuspid stenosis.

Jacob Mendez DaCosta: medical teacher, clinician, and clinical investigator.

J. M. DaCosta, a scholarly, well-trained and observant clinician, was recognized during his lifetime as a well-known authority on physical diagnosis and had an unexcelled reputation as a clinical teacher. Chairman of Medicine at the Jefferson Medical College for 19 years, president of the College of Physicians of Philadelphia in 1884 and again in 1895, he was one of the original members of the Association of American Physicians and its president in 1897. Earlier in his career, his extensive Civil War study of "a form of cardiac malady common among soldiers . . . the study of which is equally interesting to the civil practitioner" was described in his 1871 paper "On Irritable Heart; A Clinical Study of a Form of Functional Cardiac Disorder and Its Consequences." Soon labeled DaCosta's syndrome, the irritable heart lineage can be traced through the soldier's heart, the effort syndrome, and neurocirculatory asthenia in World War I, anxiety neurosis in World War II, and the mitral valve prolapse syndrome in the second half of the 20th century.

The equilibrium position of the mitral valve: an accurate model of mitral valve motion in humans.

A "semiopen" diastolic equilibrium position of the mitral valve that is assumed in the absence of transmitral flow has been demonstrated in instrumented dogs. It has been suggested that the papillary muscles and chordae tendineae play an integral role in returning the valve to this position after initial diastolic opening. To determine whether such a model of mitral valve motion is valid in noninstrumented humans without underlying valvular disease, M-mode and Doppler ultrasound studies were performed in 6 subjects who underwent prolonged periods of ventricular diastole and atrial inactivity. After maximal opening, the mitral valve assumed a stable open position in which mean separation of the anterior and posterior mitral leaflets was 52% of maximal separation. This position was maintained for a mean duration of 585 ms, during which time transmitral flow fell to 0 m/s. Peak mitral valve opening preceded the early transmitral flow peak by an average of 42 ms, suggesting an active closure of the mitral valve as flow continued to accelerate. It is concluded that a semiopen equilibrium position of the mitral valve is assumed during prolonged diastolic periods in the absence of transmitral flow and is an accurate model describing diastolic mitral valve motion in noninstrumented humans. The chordae tendineae and papillary muscles may actively participate in the genesis and maintenance of the equilibrium position.

Aortic distensibility abnormalities in coronary artery disease.

Vasodilatory capacity of nonstenotic arteries in experimental animals with atherosclerosis is decreased. It was postulated that aortic distensibility may be abnormal in patients with coronary artery disease (CAD). Aortic distensibility was determined in 24 normotensive patients with CAD and an angiographically normal aorta and values were compared with those in 18 age-matched normal subjects. Aortic diameters were measured at 3 levels--2, 4 and 6 cm above the aortic valve--by angiographic techniques. The area of the first 6 cm of the aorta above the aortic valve was planimetered and mean aortic diameters were calculated. Distensibility was calculated using the formula: [2 X (changes of the aortic diameter)/(diastolic aortic diameter) X (changes of the aortic pressure)]. CAD patients had similar aortic pressures but markedly lower distensibility than normal subjects: 0.7 +/- 0.2 vs 1.7 +/- 0.3 (p less than 0.02); 1.5 +/- 0.3 vs 4.0 +/- 0.6 (p less than 0.02); and 1.2 +/- 0.2 vs 5.3 +/- 0.6 (p less than 0.001) at 2, 4 and 6 cm above the aortic valve, respectively. Distensibility was also calculated from the mean aortic diameters and was greater in normal subjects than in CAD patients (3.4 +/- 0.4 vs 1.6 +/- 0.1, p less than 0.001). Decreased aortic distensibility in CAD may be related to the common atherosclerotic process or to reduced ascending aorta vasa vasorum flow from coronary arteries.

Evidence for progression from mild to severe mitral regurgitation in mitral valve prolapse.

Little information is available concerning the progression of mild to severe mitral regurgitation (MR) in patients with mitral valve prolapse (MVP). This study reports 86 patients, average age 60 years, who presented with cardiac symptoms, precordial systolic murmur, severe MR and a high incidence of MVP on echocardiography (57 of 75 [75%] ) and left ventriculography (61 of 84 [73%] ). Seventy-five surgically excised mitral valves appeared grossly enlarged and floppy. Histologic studies showed extensive myxomatous changes throughout the leaflets and chordae. Eighty patients had had precordial murmurs first described at average age 34 years, but the average age at which symptoms of cardiac dysfunction appeared was 59. However, once symptoms developed, mitral valve surgery was required within 1 year in 67 of 76 patients who had undergone surgery. Atrial fibrillation, present in 48 of 86 patients (56%), or ruptured chordae tendineae, present in 39 of 76 patients (51%), may have contributed to this rapid progression and deterioration. Additionally, 13 patients had a remote history of documented infective endocarditis. Twenty-eight patients had at least 1 type of serial clinical evaluation that indicated progressive MR in all 28 patients on the basis of changing auscultatory findings (24 of 26), progressive radiographic cardiomegaly (24 of 25), echocardiographic left atrial enlargement (4.3 to 5 cm in 11 patients) and angiographically worsening MR (14 of 15). Twenty-four of these patients had evidence of MVP on at least 1 of their initial studies. Thus, mild MR due to MVP and myxomatous mitral valves is a progressive disease in some patients with MVP.

Mitral valve prolapse syndrome: analysis of 62 patients aged 60 years and older.

Sixty-two patients diagnosed as having mitral valve prolapse, 60 to 81 years old, presented with disabling chest pain (20), symptoms of arrhythmias including palpitations and syncope (16), or mitral regurgitation (MR) with symptoms of congestive heart failure (26). The diagnosis of MVP was made on the basis of a combination of classic auscultatory, echocardiographic and angiographic findings. Thirteen of the 20 patients with chest pain had normal coronary angiograms and 7 had significant coronary artery disease (CAD). Patients with CAD could not be differentiated by clinical presentation alone. Furthermore, the incidence and types of arrhythmias, the presence of a positive stress test, and hemodynamic findings were similar in all patients in this group whether or not CAD was present. The 16 patients with palpitations had a broad spectrum of rhythm disorders, including both supraventricular and ventricular arrhythmias. Two patients had prehospital "sudden death" and 2 others had systemic emboli. Twenty-one of the 26 patients with MR had valve surgery. Intraoperatively the valves were described as enlarged, floppy and with redundant leaflets. Histologic examination showed extensive "myxomatous" changes throughout the valve leaflets. Thus, mitral valve prolapse is a cause of symptomatic heart disease in the elderly. It has a predictable pattern of clinical presentation and should be considered in the differential diagnosis of older patients with disabling chest pain and arrhythmias and as the cause of progressive or severe MR.

Floppy mitral valve chordae tendineae: histopathologic alterations.

Pathologic studies of floppy or myxomatous mitral valves have focused primarily on changes in the valve cusps, with little attention given to the chordae tendineae. In a systematic study of the histopathology of floppy mitral valve chordae tendineae, 128 nonruptured chordae from 8 severely regurgitant floppy mitral valves were compared to 152 chordae from 10 normal control mitral valves and to 152 chordae from 8 control mitral valves with severe regurgitation due to ischemic heart disease. Collagen alterations were observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 38% of floppy mitral valve chordae. Moderate or severe acid mucopolysaccharide accumulation was observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 39% of floppy mitral valve chordae. Nonuniform histopathologic alterations, rare in normal and control regurgitant mitral valve chordae tendineae, were frequent in floppy mitral valve chordae tendineae (p less than 0.001). Histopathologic alterations provide the basis for abnormal physical properties previously demonstrated in floppy mitral valve chordae tendineae and may predispose to chordal elongation and rupture.

An electrophysiologic study of swallowing-induced tachycardia.

Electrophysiologic studies were performed on a 73-year-old man with swallowing-induced supraventricular tachycardia, in order to define the characteristics of this unique dysrhythmia in this patient. Swallowing reliably provoked an automatic atrial focus type of atrial tachycardia, which usually changed into an atrioventricular nodal reentrant tachycardia when a critical delay in atrioventricular nodal conduction (atrio-His interval greater than or equal to 340 msec) was achieved. The atrioventricular nodal reentrant form of tachycardia did not occur spontaneously. The ease of induction and the duration of the episodes of supraventricular tachycardia were facilitated with the intravenous administration of atropine and ouabain and were decreased with administration of procainamide hydrochloride.

Intraoperative localization of intestinal arteriovenous malformation.

Intestinal arteriovenous malformation (AVM) is an uncommon cause of gastrointestinal hemorrhage and is difficult to diagnose. Selective visceral angiography is essential to make the diagnosis and to localize the lesion. We treated two patients in whom AVMs of the small intestine were located by means of arteriography and intraoperative selective mesenteric venous pressure and PO2 measurements. The local venous return from an intestinal AVM is characterized by elevated venous pressure and PO2 levels compared with the venous drainage of adjacent normal intestine.

Spontaneous aortocaval fistula with paradoxical pulmonary embolization.

The present report discusses the clinical syndrome and the management of a patient with an aortocaval fistula secondary to an abdominal aortic aneurysm. The occurrence of paradoxical pulmonary embolization with this syndrome is reported.

Mitral valve prolapse: cardiac arrest with long-term survival.

Cardiac arrest has been reported in patients with mitral valve prolapse; however, clinical characteristics and survival information are limited since most of the cases reported include autopsy data. Nine patients (2 male, 7 female) with mitral valve prolapse were identified who had cardiac arrest; ventricular fibrillation was documented in 8 patients; resuscitation was unsuccessful in 2. Eight had a history of palpitations (months to 15 years duration) and ventricular arrhythmias, 3 had a history (5-15 years) of recurrent syncope, and 1 was totally asymptomatic. Cardiac catheterization-angiographic studies in 8 patients demonstrated normal coronary artery anatomy and mitral valve prolapse. All 9 patients had auscultatory and echocardiographic evidence of mitral valve prolapse. Seven survivors (6 still alive) were followed from 3 to 14 years after cardiac arrest. A subset of patients with mitral valve prolapse and cardiac arrest is described in whom past medical history is compatible with cardiac arrhythmias or syncope, and whose long-term prognosis appears better than patients with other causes of cardiac arrest.

Valvular heart disease: the influence of changing etiology on nosology.

The many changes in classification of cardiovascular disease during the twentieth century reflect changing etiology of diseases, clinical comprehension and technological advances. In particular, the etiology of valvular heart disease has changed dramatically in the last five decades. The significant reduction of acute rheumatic fever and its sequelae, and the recognition of non-rheumatic causes of valvular disease are responsible for the metamorphosis in the etiology of valvular disorders. Valvular heart disease can be classified as follows: 1) Heritable-congenital causes of valvular heart disease e.g., floppy mitral valve with mitral valve prolapse, bicuspid aortic valve, and the Marfan syndrome; 2) Inflammatory-immunologic causes such as rheumatic fever, acquired immune deficiency syndrome, endocardial proliferative disorders, and antiphospolipid syndrome; 3) Myocardial dysfunction-ischemic cardiomyopathy, dilated or hypertrophic cardiomyopathy-resulting in valvular heart disease; 4) Diseases and disorders of other organs as causes of valvular heart disease, e.g., chronic renal failure and carcinoid heart disease; 5) Valvular heart disease related to aging: calcific aortic stenosis and mitral annular calcification; 6) Valvular disease following interventions such as valvuloplasty, valve reconstructive surgery and valve replacement; and 7) Valvular disease related to drugs and physical agents, such as chronic ergotamine use, radiation therapy and trauma. In clinical practice the most common causes of mitral regurgitation are floppy mitral valve with mitral valve prolapse, ischemic heart disease, dilated cardiomyopathy and mitral annular calcification, while the most common cause of mitral stenosis is rheumatic fever. The most common causes of isolated aortic regurgitation are bicuspid aortic valve and floppy aortic valve, while the most common causes of isolated aortic stenosis are related to the bicuspid aortic valve and the development of calcific senile aortic stenosis. The most common causes of tricuspid regurgitation are dilated cardiomyopathy, ischemic cardiomyopathy, floppy tricuspid valve with tricuspid valve prolapse and infectious endocarditis. Combined mitral and tricuspid regurgitation occur with heritable connective tissue disorders, dilated or ischemic cardiomyopathy, while the most common cause of mitral stenosis plus aortic regurgitation is rheumatic fever. Statistics obtained from cardiac surgery and necropsy may underestimate the true incidence of certain valvular diseases by selection bias. This is particularly so with valvular disease associated with significant ventricular dysfunction, or in the elderly who may not be surgical candidates, or in cases where the valvular disease is not severe enough to require surgical intervention. Recent advances in hemodynamic and imaging technology allow clinicians to define valvular structure and function and to accurately classify valvular heart disease in clinical practice.

Mitral valve prolapse: left ventricular hemodynamics in patients with chest pain, dyspnea or both.

Patients with mitral valve prolapse may present with chest pain and dyspnea. Left ventricular hemodynamics as a cause for these symptoms have not been completely evaluated in these patients. The present study was undertaken to investigate left ventricular hemodynamics in symptomatic patients with mitral valve prolapse. One hundred and three patients with mitral valve prolapse (female 72, male 31, age 56 +/- 11 years) had diagnostic cardiac catheterization for evaluation of chest pain (n = 44), dyspnea (n = 10) and for chest pain plus dyspnea (n = 49). All patients had diagnostic auscultatory findings and angiographic documentation of mitral valve prolapse. Patients with coronary artery disease and mitral regurgitation greater than mild were excluded from the study. Left ventricular end diastolic pressures before (chest pain 9.3 +/- 3.7 mmHg; dyspnea 8.2 +/- 4.2 mmHg; chest pain plus dyspnea 9.3 +/- 4.1 mmHg) and after left ventriculography (chest pain 11.6 +/- 5.5 mmHg; dyspnea 10.2 +/- 2.3 mmHg; chest pain plus dyspnea 11.7 +/- 5.6 mmHg) were normal in the majority of patients and similar in all three groups. Likewise, the left ventricular end diastolic volume index (chest pain 72.0 +/- 16 cm3, dyspnea 69.1 +/- 20 cm3, chest pain plus dyspnea 70.0 +/- 16 cm3) and ejection fraction (chest pain 64.0 +/- 8.4%, dyspnea 64.1 +/- 6.1%, chest pain plus dyspnea 64.3 +/- 6.1%) were normal in the majority of patients and similar in the three groups. Symptomatic patients with mitral valve prolapse without significant mitral regurgitation had normal left ventricular hemodynamics, and their symptoms cannot be explained on the basis of hemodynamic abnormalities alone.

Left atrial performance indices in chronic mitral valve disease.

Multidimensional left atrial (LA) performance indices have not been extensively studied in chronic mitral valve disease. LA maximal volume, stroke volume (LA volume at atrial systole minus LA minimal volume), LA ejection fraction (stroke volume/volume at atrial systole) and A-wave velocity, were measured in 14 patients with mitral stenosis (mean mitral valve area 1.5 cm2); 14 patients with chronic mitral regurgitation all in sinus rhythm; and were compared to 20 age and sex matched normal control subjects using biplane transthoracic echo and pulsed Doppler. Although LA volumes--maximal and at onset of atrial systole--were greater in mitral regurgitation and mitral stenosis (p < 0.01) compared to normal subjects, LA ejection fraction was not statistically different among the three groups. LA stroke volume was greater in mitral regurgitation and mitral stenosis compared to normal subjects, p < 0.01. LA kinetic energy (LAKE) = 1/2 mv2 (m = LA stroke volume x 1.06, blood's specific gravity, v = A wave velocity) was increased in mitral stenosis and mitral regurgitation compared to normal subjects (p < 0.001). An inverse correlation (r = 0.66, p < 0.01) was present between LAKE and mitral valve area in mitral stenosis. It is concluded that LA function, a complex interplay of multiple factors, requires multidimensional methods of analysis beyond standard measurements of size and volume, which provide additional insight into normal LA function, and better definition of LA function changes involved in the natural history of chronic mitral valve disease.