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The Canadian Cardiovascular Society is the national professional society for cardiovascular specialists and researchers in Canada. In the spring of 2004, the Canadian Cardiovascular Society Council formed the Access to Care Working Group ('Working Group') to use the best science and information available to establish reasonable triage categories and safe wait times for access to common cardiovascular procedures. The Working Group decided to publish a series of commentaries to initiate a structured national discussion on this important issue, and the present commentary proposes recommended wait times for access to echocardiography. 'Emergent' echocardiograms should be performed within 24 h, 'urgent' within seven days and 'scheduled' (elective) within 30 days. A framework for a solution-oriented approach to improve access is presented.

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OBJECTIVES: To assess the relation of left ventricular (LV) and left atrial (LA) dimensions, ejection fraction (EF) and LV mass to subsequent clinical outcome of patients with LV dysfunction enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) Registry and Trials. BACKGROUND: Data are lacking on the relation of LV mass to prognosis in patients with LV dysfunction and on the interaction of LV mass with other measurements of LV size and function as they relate to clinical outcome. METHODS: A cohort of 1,172 patients enrolled in the SOLVD Trials (n = 577) and Registry (n = 595) had baseline echocardiographic measurements and follow-up for 1 year. RESULTS: After adjusting for age, New York Heart Association (NYHA) functional class, Trial vs. Registry and ischemic etiology, a 1-SD difference in EF was inversely associated with an increased risk of death (risk ratio, 1.62; p = 0.0008) and cardiovascular (CV) hospitalization (risk ratio, 1.59; p = 0.0001). Consequently, the other echo parameters were adjusted for EF in addition to age, NYHA functional class, Trial vs. Registry and ischemic etiology. A 1-SD difference in LV mass was associated with increased risk of death (risk ratio of 1.3, p = 0.012) and CV hospitalization (risk ratio of 1.17, p = 0.018). Similar results were observed with the LA dimension (mortality risk ratio, 1.32; p < 0.02; CV hospitalizations risk ratio, 1.18; p < 0.04). Likewise, LV mass > or =298 g and LA dimension > or =4.17 cm were associated with increased risk of death and CV hospitalization. An end-systolic dimension >5.0 cm was associated with increased mortality only. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% had lower mortality) but not in the group with LV mass <298 g. CONCLUSIONS: In patients with LV dysfunction enrolled in the SOLVD Registry and Trials, increasing levels of hypertrophy are associated with adverse events. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% fared better) but not in the group with LV mass <298 g. These data support the development and use of drugs that can inhibit hypertrophy or alter its characteristics.

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BACKGROUND: Septal systolic motion is determined by the end-diastolic trans-septal pressure gradient, and hence is load dependent. OBJECTIVE: To explore septal contribution to left ventricular (LV) systolic function in patients with heart failure. DESIGN: Echocardiograms were identified post hoc from normal subjects and a cohort of patients with heart failure. PATIENTS: Twelve normal subjects and 69 patients with heart failure and normal conduction or left bundle brance block (LBBB) were studied. METHODS: Parasternal short axis LV end-diastolic and end-systolic areas were traced. Using a floating centroid, 32 radial chords were constructed, and perecentage shortening from end-diastole to end-systole was calculated for each chord. MAIN RESULTS: Comparing heart failure with normal conduction and LBBB, LV end-diastolic area was similar (43+/-10 versus 45+/-12 cm(2) not significant), but stroke area was higher in normal conduction (7+/-4 versus 4+/-4cm(2), P<0.05) as was area ejection fraction (0.17+/-0.11 versus 0.10+/- 0.08, P<0.01). In normal subjects, the summed percentage shortening of 10 midseptal chords was similar to that of 10 midfreewall chords (256+/-16% versus 235+/-32%, not significant). In contrast, patients with heart failure and normal conduction had greater midseptal than midfreewall sum med chord shortening (113+/-18% versus 60+/-12%, P<0.05); patients with heart failure and LBBB had paradoxical septal motion (3+/-28, P<0.05 compared with normal conduction). CONCLUSIONS: Patients with heart failure and normal conduction have an enhanced septal contribution to LV systolic function compared with normal subjects. In heart failure with LBBB, this is lost and the area ejection fraction is lower. Strategies to optimize septal function in heart failure warrant further study.

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BACKGROUND: Improved hemodynamics with the SPV and Freestyle bioprostheses compared to stented valves have been reported. It has been suggested that there is more aortic insufficiency (Al) with the Freestyle than with the SPV valve. This study was designed to assess the hemodynamic performance of these two valves implanted at a single institution with all echocardiograms reviewed by one echocardiographer. METHODS: From 1993 to 1997 112 patients underwent aortic valve replacement with stentless aortic valves (69 SPV, 43 Freestyle). There were no major preoperative differences in patient age, gender, NYHA class, or ejection fraction between groups. Echocardiographic assessment was obtained at discharge, 3 to 6 months following surgery, and yearly thereafter. RESULTS: Mean follow-up was 15.9 months for the SPV and 28.6 months for the Freestyle. Both valves have excellent valve areas and low transvalvar mean gradients. There is a trend for more Al in the SPV group. At 1 year, 1+ or greater Al was present in 11 of 42 SPV patients compared to 2 of 34 Freestyle patients (p = 0.030). Al has tended to remain stable over time, has not progressed, and is not clinically evident. DISCUSSION: Differences in the previously reported incidence of aortic insufficiency with these valves may have more to do with the method of reporting Al than its actual frequency. Within our institution, there has been slightly more mild Al with the SPV valve than with Freestyle. Long-term follow-up of these valves is needed to determine if the Al progresses or becomes clinically important. To date there is no such trend with either valve.

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Abnormalities of diastolic filling are increasingly recognized as a cause of symptoms and predictors of outcome in patients with most forms of heart disease. Noninvasive assessment of diastolic filling is possible in almost all patients, but accurate evaluation must relate echocardiographic Doppler measurements to the complex physiologic and hemodynamic factors responsible for normal and abnormal filling. This evaluation has been facilitated by recent correlation of Doppler measurement of mitral and pulmonary venous inflow with hemodynamic studies. These studies have confirmed that when a careful, integrated approach is taken, Doppler flow patterns can document a progressive pattern of abnormality in many conditions. Impaired left ventricular (LV) relaxation is seen early and is recognized by a decrease in early transmitral LV filling and an increased proportion of filling during atrial contraction. As abnormalities progress, increasing LV chamber stiffness and elevated left atrial pressure lead to a "pseudonormal" filling pattern that previously has caused considerable confusion. This can be unmasked by careful evaluation of pulmonary venous inflow and the use of the Valsalva maneuver. When marked diastolic abnormalities are present, LV filling has restrictive features characterized by rapid early filling, a very stiff left ventricle with high filling pressures, and a poor prognosis. Routine measurement of indexes of diastolic filling have been hampered by uncertainty as to what should be measured, what techniques should be used, definition of normal values, and a clear method of reporting findings. This report represents the efforts of a Canadian consensus group to define a national standard for the performance and reporting of echocardiographic Doppler studies of diastolic filling.

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Patients with severe left ventricular (LV) dysfunction may or may not have overt heart failure and ventricular dysrhythmia. To study factors behind this variability, we examined a subset of 311 patients from the Studies of Left Ventricular Dysfunction-95 with a history of moderate heart failure (treatment trial) and 216 with no failure (prevention trial), all with ejection fractions <0.35. Echocardiographic variables were compared between trials and also correlated with dysrhythmia in 258 patients, and with neurohormones in 199 patients. Compared with prevention patients, treatment patients had larger LV end-diastolic diameter, end-systolic volume, sphericity index, and ratio of early to late diastolic filling velocity by Doppler (E/A ratio), lower LV ejection fraction and atrial contribution to ventricular filling, and similar LV mass, end-diastolic volume, and estimates of systolic wall stress. With prevention and treatment patients combined, the prevalence of abnormally elevated atrial natriuretic peptide was 92% in the highest tertile of E/A ratio compared with 55% in the lower tertiles (p=0.006). Across tertiles of LV end-diastolic volume, there was an increase in the prevalence of nonsustained ventricular tachycardia (24%, 45%, and 45%; p=0.007) and premature ventricular complexes >10/hour (48%, 62%, and 80%; p<0.001). Thus, in severe LV dysfunction, ventricular filling indexes suggestive of high filling pressures, along with larger and more spherical ventricles, are particularly common in patients with overt heart failure, thus suggesting that diastolic properties and the degree of ventricular remodeling affect clinical status. Once ejection fraction is significantly reduced, the prevalence of ventricular dysrhythmia correlates with LV size rather than systolic function. This observation lends support to previous experimental findings on the role of myocardial stretch and scar in the genesis of dysrhythmia.

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BACKGROUND: Studies of Left Ventricular Dysfunction (SOLVD) demonstrated that enalapril therapy significantly improved the clinical course of patients with left ventricular (LV) dysfunction. The goals of this substudy were to evaluate changes in LV structure and function in SOLVD patients and to test the hypothesis that enalapril inhibits remodeling in patients with LV dysfunction. METHODS AND RESULTS: Patients entering both the prevention and treatment arms of SOLVD from 5 of the 23 clinical centers were recruited for this substudy. The 301 patients who participated underwent Doppler-echocardiographic evaluation according to standard protocol before randomization to either enalapril or placebo and again after 4 and 12 months of therapy. Recorded data were analyzed in a blinded fashion at a central core laboratory. Analysis of baseline clinical characteristics showed that patients enrolled in the substudy were generally representative of the SOLVD population, although prevention arm patients were slightly overrepresented in the substudy group (69.8% compared with 61.9% of remaining SOLVD patients). The enalapril group demonstrated significant reductions in the mitral annular E-wave-to-A-wave velocity ratio (due predominantly to a reduction in E-wave velocity), and this response was different from that seen in the placebo group (P = .030). Changes in the E-to-A ratio in the enalapril group correlated significantly with changes in plasma atrial natriuretic peptide (r = .56; P < or = .01). LV end-diastolic and end-systolic volumes increased in placebo but not enalapril-treated patients, and the differences in response between the treatment groups were significant (P = .025 and .019, respectively). LV mass tended to increase in placebo patients and to be reduced in enalapril-treated patients, and the difference in response between the groups was highly significant (P < or = .001). CONCLUSIONS: These data demonstrate that enalapril attenuates progressive increases in LV dilatation and hypertrophy in patients with LV dysfunction. The results support the possibility that the favorable effects of enalapril reported in the SOLVD trials were related to inhibition of LV remodeling.

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Alterations in left ventricular (LV) contractility, relaxation, and chamber dimensions induced by efferent sympathetic nerve stimulation were investigated in nine anesthetized open-chest dogs in sinus rhythm. Supramaximal stimulation of acutely decentralized left stellate ganglia augmented heart rate, LV systolic pressure, and rate of LV pressure rise (maximum +dP/dt, 1,809 +/- 191 to 6,304 +/- 725 mmHg/s) and fall (maximum -dP/dt, -2,392 +/- 230 to -4,458 +/- 482 mmHg/s). It also reduced the time constant of isovolumic relaxation, tau (36.5 +/- 4.8 to 14.9 +/- 1.1 ms). Simultaneous two-dimensional echocardiography recorded reductions in end-diastolic and end-systolic LV cross-sectional chamber areas (23 and 31%, respectively), an increase in area ejection fraction (32%), and increases in end-diastolic and end-systolic wall thicknesses (14 and 13%, respectively). End-systolic and end-diastolic wall stresses were unchanged by stellate ganglion stimulation (98 +/- 12 to 95 +/- 9 dyn x 10(3)/cm2; 6.4 +/- 2.4 to 2.4 +/- 0.3 dyn x 10(3)/cm2, respectively). Atrial pacing to similar heart rates did not alter monitored indexes of contractility. Dobutamine and isoproterenol induced changes similar to those resulting from sympathetic neuronal stimulation. These data indicate that when the efferent sympathetic nervous system increases left ventricular contractility and relaxation, concomitant reductions in systolic and diastolic dimensions of that chamber occur that are associated with increasing wall thickness such that LV wall stress changes are minimized.

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Left ventricular (LV) and left atrial (LA) chamber sizes are frequently used to assist in assessing the severity of mitral regurgitation (MR). To study the reliability of these measurements in the clinical setting 2-dimensional echocardiographic measurements of the left ventricle and left atrium were obtained in 92 consecutive patients with MR present on both angiography and Doppler echocardiographic examinations performed within 2.8 +/- 2.5 days of each other. The accuracy of chamber dimensions in identifying severe MR (angiographic grade 3 to 4+) was determined in the total population and the following patient subgroups: (1) isolated chronic MR with preserved LV function inclusive of all rhythms; (2) isolated chronic MR, preserved LV function and sinus rhythm; (3) isolated chronic MR with LV dysfunction; (4) chronic MR associated with other valvular disease; and (5) acute MR. Only in subgroup 2 were chamber sizes reliable in identifying severe MR. Atrial dimensions provided the most accurate assessment with an LA volume greater than 58 ml, anteroposterior dimension greater than 45 mm and superoinferior dimension greater than 55 mm, with sensitivities of 75, 75 and 88%, specificities of 83, 100 and 83%, positive predictive values of 92, 100, and 93% and negative predictive values of 56, 60, and 71%, respectively. LV dimensions had excellent positive predictive values but lower sensitivities. Normalizing for body surface area did not improve the accuracy of uncorrected dimensions. Although increased LA and LV dimensions can identify severe MR, smaller dimensions do not exclude this diagnosis. With acute MR, atrial fibrillation, LV dysfunction or associated valvular disease, these dimensions are not reliable.

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This report describes three cases of massive mobile right heart thrombus and reviews the available literature to better define the pathophysiology, natural history and most appropriate therapy of the syndrome. The clinical presentation of most patients has been severe cardiopulmonary dysfunction and the diagnosis has been made by echocardiographic study. The most likely source of these cardiac thrombi is the large systemic veins. The associated mortality risk is very high. Therapy has, heretofore, been individualized. Embolectomy has been most favored, with a survival rate of 80 percent. The role of thrombolytic therapy remains to be delineated. Therapy should, however, be initiated rapidly because of the precipitous nature of the mortality risk.

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