Thomas R. Downes

Clinical evaluation of left ventricular diastolic performance

Diastole can be divided into four phases: isovolumic relaxation, early filling, diastasis, and atrial systole. The amount of LV filling that occurs during each of these phases depends on myocardial relaxation, the passive characteristics of the LV, the characteristics of the left atrium, pulmonary veins, and mitral valve, and the heart rate. When diastolic function is normal, the net effect of these factors results in an LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics. Invasive studies can quantitate the rate of myocardial relaxation and the LV diastolic pressure-volume relation. More recently, RNA and Doppler echocardiography have been used to noninvasively evaluate diastolic performance by determining the pattern of LV diastolic filling. At rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients who do not have clinically apparent diastolic dysfunction and in normals. Furthermore, a normal pattern can occur in patients who have severe diastolic dysfunction. A reduced early diastolic filling, in the absence of pulmonary congestion, indicates the loss of diastolic reserve, since the left atrium is being used as a booster pump. This pattern of diastolic filling in a patient who has symptoms of pulmonary congestion may suggest diastolic dysfunction, even if the systolic LV performance is normal. Since diastolic filling of the LV results from a complex interplay of factors, it is unlikely that a single, easily interpreted index of LV diastolic performance will ever be developed. However, the recent development of a noninvasive evaluation of the pattern of LV diastolic filling by RNA or Doppler echocardiography is an important advance. When interpreted with an understanding of the determinants of LV filling and the patients clinical status, these noninvasive tests can contribute to the rational assessment of LV diastolic performance.

Qualitative and quantitative contrasts in the mechanisms of lumen enlargement by coronary balloon angioplasty and directional coronary atherectomy

OBJECTIVES This study was designed to define and contrast the mechanisms of lumen enlargement from coronary balloon angioplasty and directional coronary atherectomy using intracoronary ultrasound imaging in vivo. BACKGROUND The mechanisms of lumen enlargement produced by percutaneous transluminal coronary balloon angioplasty and directional coronary atherectomy are not known because the coronary artery wall has not previously been studied both before and after dilation. METHODS We used intracoronary ultrasound to quantitate coronary lumen, vessel and plaque area both before and immediately after successful coronary angioplasty (n = 30) and directional coronary atherectomy (n = 25) at the site of most severe stenosis. RESULTS Angioplasty increased lumen area by 2.80 +/- 0.25 mm2 (mean +/- SE, p < 0.0001). Eighty-one percent of this lumen gain resulted from an increase in vessel area and the remaining 19% from a reduction in plaque area. Lumen gain of individual lesions was separated into three groups: 67% had an increase in vessel area (vessel expansion), 13% had a decrease in plaque area and 20% had a combination of both. In contrast, vessel expansion contributed only 22% of the lumen gain with directional coronary atherectomy, with the majority (78%) of increase in lumen size coming from a reduction in plaque area. Directional coronary atherectomy increased lumen area from 2.36 +/- 0.05 to 7.00 +/- 0.28 mm2 (p < 0.0001). Plaque reduction was the sole mechanism in 60% of lesions, vessel expansion was the sole mechanism in 12% and a combination of both mechanisms occurred in 28%. Lumen enlargement of eccentric lesions treated with directional coronary atherectomy was more commonly associated with plaque reduction (p < 0.02), whereas eccentricity did not affect the mechanism of lumen enlargement with coronary angioplasty. CONCLUSIONS This is the first study to systematically examine the coronary artery wall in vivo at the site of a severe stenosis both before and after catheter-based interventions in humans. Lumen enlargement from coronary angioplasty occurs predominantly from vessel expansion or stretching, although a reduction in plaque area contributes to the lumen gain in many patients and is the sole mechanism in a few. Lumen gain from directional coronary atherectomy is predominantly from reduction in plaque area (probably owing to tissue removal), although vessel stretching (balloon effect) occurs and is the sole mechanism in a small minority of vessels. Plaque reduction is more common in directional coronary atherectomy of eccentric lesions.

Mechanism of altered pattern of left ventricular filling with aging in subjects without cardiac disease

The mechanism whereby aging, in the absence of cardiac disease, may alter the pattern of left ventricular (LV) diastolic filling is unknown. Accordingly, this study was designed to examine the factors that may be in part responsible for agings effect on the pattern of LV diastolic filling. The LV end-diastolic pressure-volume relation was analyzed in 11 elderly subjects (68 +/- 5 years, mean +/- standard deviation) and 15 normal young adults (31 +/- 7 years) without coronary artery disease, systemic hypertension, LV hypertrophy or abnormality of LV systolic function. After catheterization, the subjects underwent pulsed Doppler analysis of mitral flow. All had normal 2-dimensional echocardiograms without LV or valvular dysfunction. Peak early filling velocity in the elderly subjects was decreased in comparison with that in young adults (61 +/- 14 vs 83 +/- 8 cm/s, p less than 0.001) and the ratio of early and late diastolic filling velocity was reduced (0.81 +/- 0.26 vs 1.88 +/- 0.40, p less than 0.001). The isovolumic relaxation time did not differ between the elderly and young subjects (158 +/- 20 vs 146 +/- 22 ms, difference not significant). In the elderly, LV end-diastolic pressure was increased (15 +/- 7 vs 11 +/- 4 mm Hg, p less than 0.05) despite a smaller end-diastolic volume index (60 +/- 16 vs 74 +/- 18 ml/m2, p less than 0.05), indicating a shift of the passive diastolic pressure-volume relation. It was concluded that early diastolic filling is reduced in normal aged subjects, even in the absence of coronary artery disease and systolic dysfunction. This altered pattern of diastolic filling may result from a shift of the passive LV diastolic pressure-volume relation.

Diastolic mitral regurgitation in acute but not chronic aortic regurgitation: Implications regarding the mechanism of mitral closure

In acute aortic regurgitation, left ventricular pressure rises rapidly during diastole, which produces presystolic mitral valve closure. This does not occur in chronic aortic regurgitation. Since normal, nonregurgitant mitral valve closure may depend on properly coordinated atrial and ventricular contractions, we hypothesized that abnormal mitral valve closure occurring before systole in acute aortic regurgitation may produce diastolic mitral regurgitation detectable by Doppler echocardiography. Accordingly, we performed ultrasonic Doppler examination of seven patients with acute aortic regurgitation and 12 patients with chronic aortic regurgitation. Regurgitant aortic flow was severe in all cases. Doppler sampling within the left atrium demonstrated regurgitant mitral flow in late diastole in all patients with acute aortic regurgitation. The onset of diastolic mitral regurgitation coincided with mitral valve preclosure in patients with acute aortic regurgitation and occurred regardless of the position of the mitral leaflets at the initiation of closure. In contrast, none of the 12 patients with chronic aortic regurgitation had mitral valve preclosure or diastolic mitral regurgitation (p less than 0.05 versus acute aortic regurgitation). We conclude that diastolic mitral regurgitation accompanies mitral valve preclosure, which occurs in acute but not chronic aortic regurgitation. Thus diastolic mitral regurgitation may be a Doppler sign of acute aortic regurgitation, in the absence of a markedly prolonged PR interval. Furthermore, this observation suggests that normal, nonregurgitant mitral closure requires more than an increase in left ventricular pressure above left atrial pressure, regardless of the position of the mitral leaflets before closure.

Magnetic resonance imaging evaluation of recipient for cryopreserved aortic allograft

Aortic valve replacement with a cryopreserved aortic allograft is the procedure of choice for many patients with aortic valvular heart disease. We have used magnetic resonance imaging preoperatively to determine annular size and coronary artery orientation in the recipient, which not only has enabled us to select an allograft of appropriate size from a distant tissue bank, but also has helped us to identify preoperatively the recipient with a truly bicuspid valve in which the coronary arteries are oriented 180 degrees apart. Sixteen consecutive patients were evaluated preoperatively, the aortic annulus being measured with both magnetic resonance imaging and echocardiography. Cryopreserved aortic allografts were ordered on the basis of the magnetic resonance imaging measurement. Annular size was then measured intraoperatively with calibrated sizers. Magnetic resonance imaging annular measurements correlated highly with those found at operation (r = 0.92), whereas echocardiographic measurements correlated less well (r = 0.69). Coronary orientation was accurately predicted in every case (r = 1.0). Therefore, we have found magnetic resonance imaging to be useful in the preoperative evaluation of patients for aortic valve replacement with a cryopreserved aortic allograft.

Perforation of the Anterior Mitral Leaflet Caused by Aortic Valve Endocarditis: Diagnosis by Two-dimensional, Transesophageal Echocardiography and Color Flow Doppler

Perforation of the mitral valve as a result of aortic valve endocarditis is rare. Recognition of such abnormality is very important before surgical intervention. Diagnosis is very difficult by either invasive or noninvasive techniques. This report stresses the role of echocardiography in evaluating this rare abnormality. Perforation of the anterior mitral valve leaflet developed in our patient as a complication of aortic valve endocarditis. The perforation was suggested by the surface echocardiogram (as an interruption of the leaflet continuity) and by the color flow Doppler (which suggested turbulent flow at the area of suspected interruption). The perforation was confirmed during surgery by transesophageal echocardiography and alerted the surgeon to repair, rather than replace, the valve.

FOUR-YEAR RESULTS OF THE PLATINUM RANDOMIZED TRIAL: CAN STENT METAL ALLOY COMPOSITION AND DESIGN AFFECT LATE CLINICAL OUTCOMES?

In the PLATINUM randomized controlled trial, the PROMUS Element Everolimus Eluting Stent (PtCr-EES) was non-inferior to the cobalt chromium PROMUS/XIENCE V EES (CoCr-EES) for the primary endpoint of target lesion failure (TLF) at 1 year. Although the stents have similar polymer, drug and drug