The velocity of circumferential fiber shortening (Vcf) is an index of myocardial performance which, although sensitive to contractile state, has limited usefulness because of its dependence on left ventricular loading conditions. This study investigated the degree and velocity of left ventricular fiber shortening as it relates to wall stress in an attempt to develop an index of contractility that is independent of preload and heart rate while incorporating afterload. Studies were performed in 78 normal subjects using M-mode echocardiography, phonocardiography and indirect carotid pulse tracings under baseline conditions. In addition, studies were performed on 25 subjects during afterload augmentation with methoxamine, 8 subjects before and during afterload challenge after increased preload with dextran and 7 subjects with enhanced left ventricular contractility with dobutamine. The relation of end-systolic stress to the velocity of fiber shortening and to the rate-corrected velocity of shortening (corrected by normalization to an RR interval of 1) was inversely linear with correlation coefficients of -0.72 and -0.84, respectively. Alterations in afterload, preload or a combination of the two did not significantly affect the end-systolic wall stress/rate-corrected velocity of shortening relation, whereas during inotropic stimulation, the values were higher, with 94% of the data points above the normal range. Age did not appear to affect the range of normal values for this index. In contrast, the end-systolic wall stress/fractional shortening relation was not independent of preload status, responding in a manner similar to that seen with a positive inotropic intervention. Thus, the velocity of circumferential fiber shortening normalized for heart rate is inversely related to end-systolic wall stress in a linear fashion. Accurate quantitation can be performed by noninvasive means and a range of normal values determined. This index is a sensitive measure of contractile state that is independent of preload, normalized for heart rate and incorporates afterload. In contrast, the end-systolic wall stress/fractional shortening relation is dependent on end-diastolic fiber length in the range of physiologically relevant changes in preload.

SUMMARY No data are available on determining right atrial and right ventricular size by two-dimensional echocardiography. We performed two-dimensional echocardiograms on eight human right-heart casts obtained at autopsy and on 50 patients who underwent complete left-and right-heart catheterization. Measurement of individual dimensions of the long and short axes of the right atrium and ventricle from right heart casts closely correlated with the volume of these structures as determined by water displacement. Further, individual dimensions by cross-sectional echo correlated well with actual casts dimensions. Subsequently, echocardiographic measurements of right atrial and ventricular long and short axes were obtained in the apical fourchambered view in a group of normals and compared with a group of patients with right ventricular volume overload states. Mean values for right atrial short-axis and long-axis measurements were greater in right ventricular volume overload patients than in normals: 6.5 ± 0.3 vs 3.6 ± 0.1 cm, and 6.0 ± 0.3 vs 4.2 ± 0.1 cm, respectively (both p < 0.001). In addition, measurements of both individual dimensions as well as planed area of the right ventricle were greater in right ventricular volume overload patients than in normals: maximal short axis 6.1 ± 0.3 vs 3.5 ± 0.2 cm, mid-short axis 6.1 ± 0.4 vs 2.8 ± 0.2 cm, and area 40 ± 2.6 vs 18 ± 1.2 cm' (all p < 0.001). There were no differences in right ventricular long-axis measurement. Two-dimensional echocardiography provided better separation of normals from right ventricular volume overload patients than did M-mode techniques. Thus, two-dimensional echocardiography, with the apical four-chambered view, enables accurate visualization of the right atrium and ventricle in almost all patients. Further, measurements of right atrial and right ventricular size by two-dimensional echocardiography readily distinguish normal patients from those with right ventricular volume overload.M-MODE ECHOCARDIOGRAPHY has dramatically altered cardiac diagnostics by providing a noninvasive method of documenting the presence of a variety of cardiac disorders, including valvular heart disease,1 2 cardiac myxomas,3 and pericardial effusion.4 This technique also permits accurate atraumatic determination of left atrial and left ventricular dimensions.5 " One area in which M-mode echocardiography has not been important, however, is in evaluating the right-sided cardiac chambers. Because of an inaccessible intrathoracic position and an irregular geometrical shape, the right atrium and right ventricle are difficult structures from which to obtain reproducible echographic signals by M-mode examination.Recently, two-dimensional echocardiographic methods have been developed which can provide a 30-80°sector arc image of cardiovascular structures.7`9 The spatial orientation afforded by such techniques has enabled cardiac imaging from new thoracic windows. Thus, with the ultrasound transducer positioned at the cardiac apex and directed toward the right shoulder, a simulta...

Variations in Ca2+ are directly correlated with clinically significant changes in myocardial contractility.

Few data are available regarding the effects of exercise training upon cardiac structure and performance in man. We evaluated the echograms of 24 normals before (PRE) and after (POST) 11 weeks of endurance exercise training. Conditioning consisted of a walk-jog-run protocol at 70% maximal heart rate for one hour four days per week. Training reduced heart rate and increased maximal duration and estimated oxygen consumption of treadmill exercise. Compared to PRE, the echogram in the POST training period revealed an increased left ventricular (LV) end-diastolic dimension (EdD), a decreased end-systolic dimension (EsD) and thus an increased stroke volume (EdD3-EsD3) and shortening fraction (EdD-EsD)/EdD). Cardiac output (CO) and peripheral vascular resistance (BP/CO X 80) were identical PRE and POST conditioning. Importantly, an increase in mean fiber shortening velocity was observed POST training as were increases in LV wall thickness, ECG voltage of S in V1 + R in V5, and LV mass. Thus endurance training was accompanied by increases in both LV dimension and mass as well as LV shortening fraction and contraction velocity as observed by echocardiogram.

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BackgroundTo evaluate the diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers in patients with probable cerebral amyloid angiopathy (CAA) according to the modified Boston criteria in a retrospective multicentric cohort.MethodsBeta-amyloid 1-40 (Aβ40), beta-amyloid 1-42 (Aβ42), total tau (t-tau), and phosphorylated tau 181 (p-tau181) were measured in 31 patients with probable CAA, 28 patients with Alzheimer’s disease (AD), and 30 controls. Receiver-operating characteristics (ROC) analyses were performed for the measured parameters as well as the Aβ42/40 ratio to estimate diagnostic parameters. A meta-analysis of all amenable published studies was conducted.ResultsIn our data Aβ42/40 (AUC 0.88) discriminated best between CAA and controls while Aβ40 did not perform well (AUC 0.63). Differentiating between CAA and AD, p-tau181 (AUC 0.75) discriminated best in this study while Aβ40 (AUC 0.58) and Aβ42 (AUC 0.54) provided no discrimination. In the meta-analysis, Aβ42/40 (AUC 0.90) showed the best discrimination between CAA and controls followed by t-tau (AUC 0.79), Aβ40 (AUC 0.76), and p-tau181 (AUC 0.71). P-tau181 (AUC 0.76), Aβ40 (AUC 0.73), and t-tau (AUC 0.71) differentiated comparably between AD and CAA while Aβ42 (AUC 0.54) did not. In agreement with studies examining AD biomarkers, Aβ42/40 discriminated excellently between AD and controls (AUC 0.92–0.96) in this study as well as the meta-analysis.ConclusionThe analyzed parameters differentiate between controls and CAA with clinically useful accuracy (AUC &gt; ∼0.85) but not between CAA and AD. Since there is a neuropathological, clinical and diagnostic continuum between CAA and AD, other diagnostic markers, e.g., novel CSF biomarkers or other parameters might be more successful.

Despite similar degrees of left ventricular systolic hypertension shortening characteristics are usually greater in patients with congenital valvular aortic stenosis (VAS) than in patients with coarctation of the aorta (CoA). We hypothesized that these dissimilarities were caused by differences in myocardial mechanics rather than by alterations in contractile state. Eleven patients with VAS (ages 6 to 41 years) and 11 with CoA were matched for age, body surface area, and peak systolic ejection gradient. Results were compared with data from 22 normal subjects matched for age and body surface area. Echocardiographic tracings of the left ventricle were recorded in conjunction with left ventricular pressure measurements (VAS) or calibrated carotid pulse tracings (CoA and normal subjects). Peak and end-systolic wall stresses as well as left ventricular shortening fraction (%AD) and rate-corrected velocity of fiber shortening (Vcfc) were calculated. No differences for left ventricular dimensions, heart rate or peak wall stress were present. Ventricular peak systolic pressures and wall mass were higher for the patients with VAS or CoA than for the normal subjects (p < .001). These parameters did not differ between the VAS and CoA groups. The patients with VAS had higher %fD and Vcfc than either the CoA or normal groups (p < .01). Afterload, as quantified by end-systolic stress, was 41% lower than normal for the patients with VAS (p < .001) and 13% higher than normal for those with CoA (p < .05). Left ventricular contractility as assessed by load-independent indexes (i.e., end-systolic stress/WAD and end-systolic stress/Vcf, relationships) was depressed in three of 11 patients with CoA. All of these patients were over 20 years of age. In contrast, the increased systolic performance noted in the patients with VAS was caused by reduced afterload at end-systole rather than by altered contractile state. Thus the extent and velocity of left ventricular shortening is lower in patients with CoA than in those with VAS because of disadvantageous afterload conditions and/or an age-related depression in contractile state. Circulation 72, No. 3, 515-522, 1985. PATIENTS wth congenital valvular aoartic stenosis (VAS) or coarctation of the aorta (CoA) have left ventricular pressure overload resulting in concentric ventricular hypertrophy. The stimulus for hypertrophy in both of these lesions is believed to be the peak forces (i.e., wall stress) acting on the myocardial fibers during systole.'-7 The ventricle responds by increasing wall thickness until peak systolic wall stress is normalized.2' 3 Despite a similar hypertrophic response to long-term pressure overload, the left ventricle in patients with VAS is frequently hyperkinetic when compared with that in patients with CoA.7-'l Indeed, chil-

Ambulatory monitoring and maximal treadmill exercise were compared in 40 normal subjects and 31 patients with mitral prolapse. A variable arrhythmia spectrum was observed in prolapse during monitoring: premature ventricular contractions in 18 (58%), supraventricular arrhythmias in 11 (35%), and bradyarrhythmias in 9 (29%). Significantly less arrhythmias occurred in normal subjects during monitoring: 10 (25%, P greater than 0.001), 3 (8%, P less than 0.001), 4 (10%, P less than 0.05), and 2 (5%, P less than 0.02), respectively. In patients with prolapse, arrhythmias occurred on resting electrocardiogram (ECG), 35% premature ventricular contractons, 6% supraventricular arrhythmias, and 10% bradyarrhythmias, and on treadmill exercise, 45%, 10%, and 3%; therefore, ambulatory monitoring was the most sensitive method of arrhythmia detection. No correlation existed between clinical features of prolapse and arrhythmias. Thus, arrhythmias occur in most patients with mitral prolapse, are not predictable by clinical characteristics, comprise a spectrum of ventricular and supraventricular tachyarrhythmias and bradyarrhythmias, and are best detected by ambulatory ECG monitoring.