Predictors of mortality in end-stage renal disease patients with mitral annulus calcification.

OBJECTIVE: Mitral annulus calcification (MAC) is an independent predictor of cardiovascular mortality in the general population. The purpose of the current historical cohort study is to assess risk factors for long-term mortality in end-stage renal disease (ESRD) patients with MAC (n = 30; age, 62 +/- 2 yr), as compared to ESRD patients without MAC (n = 30; age, 63 +/- 2 yr). Additional analysis compared ESRD patients with MAC to non-ESRD patients with MAC (n = 32; age, 66 +/- 2 yr). METHODS: The groups included age-matched male patients followed at a single center. Long-term survival was assessed by Kaplan-Meier analysis. Regular and stepwise Cox proportional hazards models were used to determine risk factors for mortality. RESULTS: There was a similarly high prevalence of cardiovascular complications, including hypertension, coronary artery disease, left ventricular hypertrophy, atrial fibrillation, and congestive heart failure, in all three groups. Median survival time was significantly longer in non-ESRD patients (90 months), compared with the ESRD with MAC (45 months) and ESRD without MAC (45 months) patients (log-rank test; P < 0.001). With stepwise Cox proportional hazards model, including ESRD patients with MAC and ESRD patients without MAC, increased calcium x phosphate product, decreased serum creatinine concentration, and the presence of coronary artery disease and lower extremity amputations were independent predictors of mortality for patients with ESRD. With stepwise Cox proportional hazards model, including ESRD patients with MAC and non-ESRD patients with MAC, the presence of ESRD, atrial fibrillation, diabetes, aortic valve calcification, coronary artery disease, and tricuspid regurgitation were independent predictors of mortality. CONCLUSION: The mortality rate was high in ESRD patients, approximately 15% per year. After accounting for baseline cardiovascular disease and traditional risk factors, the presence of MAC did not confer additional risk for mortality.

Left ventricular papillary muscle morphology and function in left ventricular hypertrophy and left ventricular dysfunction.

BACKGROUND: This study was prospectively performed to evaluate the anatomy and contractile performance of LV papillary muscles (PM) in humans using transesophageal echocardiography (TEE), and to determine the relationship between PM anatomy and contractile function in normal left ventricle (LV), left ventricular hypertrophy (LVH) and systolic dysfunction. MATERIAL AND METHODS: TEE examinations were prospectively performed in 153 patients. End-diastolic (ED) and end-systolic (ES) cross sectional areas of both PMs were obtained at the transgastric mid papillary short axis views. ED and ES lengths of PMs were obtained from the transgastric long axis views, and fractional systolic shortening (FS) was calculated. PM shape description was derived from the formula Area/L2. LV EF, wall thickness and mass were determined from transthoracic echocardiographic measurements. RESULTS: The % FS in patients with normal EF (>55%) was 21.1 +/- 9.1% for anterior PM (APM) and 17.1 +/- 6.2% for posterior PM (PPM). The values for hypertrophic LV were as follows; 25.2 +/- 8.1 (APM) and 15.8 +/- 5.6 (PPM), for dilated cardiomyopathy, 15.0 +/- 6.8 (APM) and 13.4 +/- 4.2 while values for non-dilated cardiomyopathy were 15.6 +/- 8.0 and 11.3 +/- 6.0 respectively. In dilated cardiomyopathy patients, both PM lengths were significantly longer (p<0.05) and thinner (p<0.05) than in patients with normal EF. In the hypertrophied LV, the PMs were thicker (p<0.05) and had larger cross sectional areas p<0.05. CONCLUSIONS: TEE is a safe and useful method for detailed study of PM morphology and contractile performance in living humans with normal or impaired LV systolic function. Quantitative TEE data on PM geometry, size, and contractile function are presented here for the first time.

Echocardiography of serous effusions adjacent to the heart.

Sonolucent spaces in close proximity to the heart are common in routine clinical echocardiographic practice, yet apart from pericardial effusions have received little attention. These clear spaces can represent left or right pleural effusions, ascites, pericardial cysts, or unusual diaphragmatic hernias. All these entities have typical echocardiographic features, including location, size, shape, and anatomic relationships to contiguous structures. In addition, loculated pericardial effusions, with or without associated tamponade, have to be considered in the differential diagnosis. In this brief review, we discuss and illustrate these various types of juxtacardiac sonolucencies.

Papillary muscle contribution to ventricular ejection in normal and hypertrophic ventricles: a transesophageal echocardiographic study.

BACKGROUND: The interrelationship between left ventricular (LV) volume, stroke volume, and papillary muscle (PM) volume have not been studied. These volumes are relevant in understanding LV ejection mechanics in normal chambers and ascertaining whether differences exist between normal and hypertrophied LV chambers. METHODS AND RESULTS: PM basal areas were measured in short-axis transesophageal echocardiographic views and lengths were measured in long-axis views. PM volume was estimated by the formula for volume of a cone: 1/3 x PM base area x PM length. The formula for LV volume was as follows: LV volume = 2/3 x LV area x LV length. Of the initial 82 subjects with normal LV function studied by TEE, data on 71 are presented in this report. Thirty-two patients had normal LV size and wall thickness, and 39 had LV hypertrophy (LVH). PM volume/LV volume % in end-diastole (ED) and end-systole (ES) in normal muscles was 3.1 +/- 1.0 and 9.6 +/- 4.9, respectively. In LVH, the respective values were 5.1 +/- 2.0 (P < 0.05) and 13.5 +/- 4.9 (P < 0.05). For those with severe LVH, the values were 7.1 +/- 2.5 (P < 0.001) and 15.9 +/- 4.1 (P < 0.001), respectively, for ED and ES. Similar trends were seen in the PM volume/stroke volume relationships in normal and hypertrophic ventricles. CONCLUSIONS: PMs are larger and form a larger fraction of LV volume in LVH than in normal muscles. In patients with severe LVH, the contribution of PMs to ventricular ejection is more pronounced. PMs may, therefore, play a larger role in LV ejection in LVH than in normal ventricles (i.e., hypertrophied PM enhance the pump efficiency of LV ejection).

Transesophageal echocardiographic spectrum of calcific mitral abnormalities in patients with end-stage renal disease.

This report provides a morphological description of atypical and unusual mitral and submitral calcifications in patients with end-stage renal disease. The use of transesophageal echocardiography (TEE) with enhanced image quality and resolution has made possible a detailed evaluation of the distribution and echocardiographic morphology of mitral calcification in end-stage renal disease. To our knowledge, there has been no such prior report with TEE. Our TEE observations reveal that in addition to the common well known posterior mitral annulus calcification, the following varieties of calcification also exist: basal calcification of both mitral leaflets with sparing of free edges, calcification in the intervalvular fibrosa region, and small calcific excrescences at the bases of both mitral leaflets. These abnormalities have previously received little or no attention.

Echocardiography of the coronary sinus in adults.

The coronary sinus (CS) is a small tubular structure just above the posterior left atrioventricular junction. The CS can be imaged in several different echocardiographic views. Using zoom M-mode recordings of the CS in apical two-chamber view, CS caliber can be sharply imaged and easily measured during different phases of the cardiac cycle. We have recently shown that the CS narrows during atrial contraction in persons with sinus rhythm, but does not narrow at all if atrial fibrillation is present. Attenuation of CS narrowing occurs in patients with congestive heart failure and inferior vena cava plethora. Maximal CS caliber occurs during ventricular systole. Patients with poor left ventricular systolic function show mild CS dilatation. Greater CS dilatation is present in patients with persistent left superior vena cava, and huge dilatation when this anomaly is accompanied by absence of a right superior vena cava. Injection of sonicated saline into a left and then a right arm vein is diagnostically useful in confirming these two venous anomalies. Pulsed-wave Doppler of the CS can be recorded in the parasternal right heart inflow view. From this and from the CS cross-section area it may be possible to estimate coronary blood flow.

Dynamic cyclic changes in coronary sinus caliber in patients with and without congestive heart failure.

M-mode echography of the coronary sinus in the apical 2-chamber view enabled us to measure coronary sinus caliber at specific phases of the cardiac cycle. Coronary sinus narrowing occurs consistently during atrial contraction, but is always absent in atrial fibrillation; in patients with congestive heart failure and systemic venous congestion, this narrowing is significantly attenuated.

The vital role of papillary muscles in mitral and ventricular function: echocardiographic insights.

The two left ventricular (LV) papillary muscles are small structures but are vital to mitral valve competence. Partial or complete rupture, complicating acute myocardial infarction, causes severe or even catastrophic mitral regurgitation, potentially correctable by surgery. Papillary muscle dysfunction is a controversial topic in that the role of the papillary muscle itself, in causing mitral regurgitation post infarction, has been seriously questioned; it is less confusing if this syndrome is attributed not only to papillary muscle but also to adjacent LV wall ischemia or infarction. Papillary muscle calcification is easily and frequently detected on echocardiography, but its clinical significance remains uncertain. Papillary muscle hypertrophy accompanies LV hypertrophy of varied etiology and may have a significant role in producing dynamic late-systolic intra-LV obstruction in hypertrophic cardiomyopathy and other hyperdynamic hypertrophied LV chambers. All the above abnormalities can be adequately assessed by 2-D echocardiography and the Doppler modalities. In selected cases, transesophageal echocardiography can provide additional valuable data by improving visualization of papillary muscles and mitral apparatus.

Progression to calcific mitral stenosis in end-stage renal disease.

A 59-year-old man with end-stage renal disease and on hemodialysis had neither mitral stenosis nor mitral calcification on echo-Doppler examination in 1989, but had extensive mitral calcification and definite mitral stenosis on conventional and transesophageal echocardiography in 1994. The left ventricle had marked concentric hypertrophy. To our knowledge this is the first documentation of the development of calcific mitral stenosis in end-stage renal disease revealed by serial echo-Doppler studies.

Echocardiographic manifestations of mediastinal masses compressing or encroaching on the heart.

Because of its central position within the thorax, the heart can be encroached upon by masses originating in either anterior, posterior, or superior mediastinum. A distinction may be made between (A) Encroachment: distortion or partial displacement of one or more cardiac chambers by a contiguous mediastinal mass, without adverse hemodynamic effects, and (B) Compression: resulting in clinical manifestations similar to tamponade. Transthoracic and, recently, transesophageal echocardiography have been found useful in detecting mediastinal masses, the information obtained being complementary or preliminary to more complete imaging by CT or MRI. Anterior masses tend to compress the right heart chambers; posterior masses impinge on or compress the left atrium or ventricle, particularly the former. The wide variety of echographic appearances are briefly reviewed. Recently TEE has made it possible to diagnose masses obstructing the superior vena cava or pulmonary veins. A common, though little known, type of posterior mediastinal encroachment that echocardiographers need to be aware of is that of abnormal esophageal/gastric masses including hiatus hernia and esophageal carcinoma, which have typical two-dimensional echo features and may sometimes simulate left atrial masses.

Coronary artery disease, myocardial infarction, and brain embolism.

The incidence of in-hospital stroke complicating acute myocardial infarction is approximately 1%. This rate is largely unaffected by thrombolytic therapy. Large myocardial infarctions, anterior wall involvement, prior stroke, and increasing age are risk factors for ischemic stroke. Left ventricular thrombi commonly occur with anterior wall infarctions. There is some evidence that anticoagulation reduces their incidence and uncontrolled studies suggest that anticoagulation may reduce the risk of embolization. Left ventricular aneurysms have a low rate of embolization and do not require systemic anticoagulation. Treatment of acute myocardial infarction with t-PA and anisoylated plasminogen streptokinase activator complex are associated with a higher risk of stroke than treatment with streptokinase; this excess risk is attributable to an increased rate of cerebral hemorrhages.

Problems and pitfalls in the echocardiographic assessment of pericardial effusion.

The echocardiographic diagnosis of pericardial effusions is usually based on visualization of a sonolucent circumcardiac space of varying width. However, potential fallacies in interpretation can arise if sonolucent spaces adjacent to the heart (pleural effusions, ascites, pericardial cysts) are mistaken for pericardial effusions. Loculated pericardial effusions, especially if unusual in location or configuration, can cause diagnostic difficulty on occasion. The differential diagnosis of various "solid" echoes within a pericardial effusion is of clinical relevance, yet not widely discussed. Inflammatory tissue, neoplastic involvement, pus, caseous material, and extravasated blood all have characteristic echocardiographic morphologies. All of the various reported echocardiographic signs of tamponade do not have the same significance, so that caution is necessary not to over- or under-read tamponade. Chamber collapse can be absent in real tamponade in specific situations. On the other hand, "regional" tamponade can occur if loculated pericardial effusions are sufficiently large and high tension; echocardiographic appearances are "atypical" but diagnostically valuable if correctly interpreted. These and certain other unusual variants of tamponade deserve to be better known among echocardiographers not only because of their intrinsic interest, but also to avoid potential pitfalls in the echocardiographic assessment of patients with suspected disease.

Pericardial complications of cardiac surgery: emphasis on the diagnostic role of echocardiography.

Pericardial effusions are common following cardiac surgery; uncommonly they are large in size and may cause tamponade, either in the early or late postoperative period. Such effusions causing tamponade may be circumcardiac, but are frequently loculated, in which case one or more cardiac chambers is selectively compressed. Fortunately, echocardiography is capable of imaging not only the presence, location, and size of the pericardial effusion, but also indicating the presence of tamponade. Constrictive pericarditis resulting from cardiac surgery is being recognized with increasing frequency and has been associated with various echocardiographic abnormalities. This review also discusses certain other pericardial complications of cardiac surgery including supraventricular arrhythmias, chylopericardium, and posttransplant problems.