Sex-related difference in regression of left ventricular hypertrophy with antihypertensive treatment: the LIFE study.

While left ventricular (LV) structure and function differ between hypertensive women and men, it remains unclear whether sex affects regression of LV hypertrophy with antihypertensive treatment. We analysed paired echocardiograms in 500 men and 347 women enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study at baseline and after 12 months of antihypertensive treatment with either losartan or atenolol. At enrollment, 177 women and 242 men were randomized to losartan-based treatment and 161 women and 247 men were randomized to atenolol-based treatment (sex difference=NS). After 12 months of antihypertensive treatment, blood pressure was lowered similarly in women (152/83 from 174/97 mmHg) and men (149/85 from 173/99 mmHg; both P<0.001, sex difference=NS), without significant change in body weight in either sex. Cardiac output and pulse pressure/stroke volume were equivalently reduced in both sexes (-0.2 vs -0.1 l/min and both -0.20 mmHg/ml/m(2), respectively; both P=NS). Absolute LV mass change after 12 months of antihypertensive treatment was greater in men than in women (-30 vs -24 g, P=0.01). However, after adjusting for baseline LV mass and randomized study treatment, LV mass reduction was greater in women than in men (-33 vs -23 g, P=0.001). LV mass regression was greater in women, by 8.0+/-2.8 g, after adjusting for baseline LV mass and randomized study treatment. After consideration of baseline LV mass and randomized study treatment, antihypertensive treatment regressed LV hypertrophy more in women. Further studies are needed to identify the mechanisms and prognostic implications of this sex-related difference.

Impact of coronary artery disease on left ventricular systolic function and geometry in hypertensive patients with left ventricular hypertrophy (the LIFE study).

Hypertensive patients with left ventricular (LV) hypertrophy have a higher incidence of cardiovascular events than those without it. We hypothesized that a close relation exists between clinical evidence of coronary artery disease (CAD) and alterations in LV structure and function that contribute to their higher risk. Echocardiograms were recorded in 963 hypertensive patients (mean age 66 +/- 7 years, 41% women) with electrocardiographic LV hypertrophy, and divided into 149 with and 814 without clinical (prior myocardial infarction or angina pectoris) or electrocardiographic (Minnesota codes 1.1, 1.2) evidence of CAD. Patients with CAD had larger LV internal dimensions (5.5 +/- 0.6 vs 5.2 +/- 0.5 cm), increased LV mass (136 +/- 31 vs 122 +/- 24 g/m(2), and 62.4 +/- 19.4 vs 55.5 +/- 12.1 g/m(2.7)), lower ejection fraction (58 +/- 10% vs 62 +/- 8%), higher circumferential end-systolic wall stress (cESS) (198 +/- 59 vs 181 +/- 47 kdynes/cm(2), all p <0.001), and higher total peripheral resistances (2,088 +/- 628 vs 1,963 +/- 553 dynes x s x m(2)/cm(3), p = 0.02). Although eccentric LV hypertrophy predominated, the CAD group had a greater prevalence of this geometric pattern than the non-CAD group (56% vs 47%, p <0.02). An index of myocardial oxygen demand per beat--the LV mass x cESS x ejection time--was 20% higher in patients with CAD. In conclusion, clinical evidence of CAD in hypertensive patients with electrocardiographic evidence of LV hypertrophy identifies subjects with structural and functional abnormalities at high risk for cardiovascular events. LV mass. cESS. ejection time, a noninvasive index that parallels myocardial oxygen demand per beat, is especially high in hypertensive patients with CAD.

Effect of regression of left ventricular hypertrophy from systemic hypertension on systolic function assessed by midwall shortening (HOT echocardiographic study).

Depressed midwall shortening has been shown to be an independent predictor of cardiovascular morbid events in hypertensive patients with left ventricular (LV) hypertrophy despite normal endocardial fractional shortening. The effects of LV mass changes in hypertensive patients on midwall shortening are unclear. To determine the impact of LV hypertrophy regression on LV systolic function assessed at the endocardium and the midwall level, 508 patients (58% men, 57% Caucasians, mean age 60 +/- 7 years) participating in the Hypertension Optimal Treatment study were prospectively studied by serial echocardiography at baseline, year 1, year 2, and at the end of the study. The Hypertension Optimal Treatment study was designed to challenge the existence of the J-curve phenomenon in hypertension. This study enrolled men and women between 50 and 80 years of age with mild to moderate hypertension. Patients were treated with a regimen based on felodipine with the addition of other antihypertensive drug classes as needed to reduce the diastolic blood pressure to a predefined target of < or =80, < or =85, or < or =90 mm Hg. From baseline to year 1, year 2, and end of the study, body mass index was unchanged (30.4, 30.1, 30.2, and 30.5 kg/m(2)); however, diastolic blood pressure was significantly reduced (99, 83, 80, and 80 mm Hg, p <0.0001), as was systolic blood pressure (161, 139, 137, and 134 mm Hg, p <0.0001) and LV mass index (117, 119, 107, and 106 g/m(2), p <0.0001). Over the same period of observation the endocardial fractional shortening did not change significantly (40%, 42%, 43%, and 44%); however, shortening at the midwall level showed improvement (20%, 21%, 22%, and 30%, p <0.001). In conclusion, midwall shortening is a more sensitive index of systolic function in subjects with pressure-overload hypertrophy, and it identifies high-risk patients who may benefit from a more aggressive antihypertensive program. The disparity between midwall and endocardial shortening suggests reduced myofibril function in patients with hypertension-induced hypertrophy.

Pulmonary artery systolic pressures estimated by echocardiogram vs cardiac catheterization in patients awaiting lung transplantation.

BACKGROUND: At many lung transplant centers, right heart catheterization and transthoracic echocardiogram are part of the routine pre-transplant evaluation to measure pulmonary pressures. Because decisions regarding single vs bilateral lung transplant procedures and the need for cardiopulmonary bypass are often made based on pulmonary artery systolic pressures, we sought to examine the relationship between estimated and measured pulmonary artery systolic pressures using echocardiogram and catheterization, respectively. METHODS: We retrospectively reviewed all patients in our program who had measured pulmonary hypertension (n = 57). Patients with both echocardiogram-estimated and catheterization-measured pulmonary artery systolic pressures performed within 2 weeks of each other were included (n = 19). We analyzed results for correlation and linear regression in the entire group and in the patients with primary pulmonary hypertension (n = 8) and pulmonary fibrosis (n = 8). RESULTS: In patients with primary pulmonary hypertension, pulmonary artery systolic pressure was 94 +/- 27 and 95 +/- 15 mm Hg by echocardiogram and catheterization, respectively, with r(2) = 0.11; in patients with pulmonary fibrosis, 57 +/- 23 and 58 +/- 12 mm Hg with r(2) = 0.22; and in the whole group, 76 +/- 29 and 75 +/- 23 mm Hg with r(2) = 0.50. Thirty-two additional patients had mean pulmonary artery systolic pressure = 48 +/- 16 mm Hg by catheterization but either had no evidence of tricuspid regurgitation by echocardiogram (n = 22) or the pulmonary artery systolic pressure could not be measured (n = 10). CONCLUSIONS: In patients with pulmonary hypertension awaiting transplant, pulmonary artery systolic pressures estimated by echocardiogram correspond but do not serve as an accurate predictive model of pulmonary artery systolic pressures measured by catheterization. Technical limitations of the echocardiogram in this patient population often preclude estimating pulmonary artery systolic pressure.

Calculation of lung flow differential after single-lung transplantation: a transesophageal echocardiographic study.

Single-lung transplantation (SLT) is a viable option for patients with end-stage pulmonary disease. After successful SLT, pulmonary blood flow is preferentially shifted to the transplanted lung, creating a flow differential. Lack of flow differential may be indicative of potential vascular complications such as anastomotic stenosis or thrombosis. To assess the ability of transesophageal echocardiography (TEE) in estimating lung flow differential in patients undergoing SLT, biplane TEE was prospectively performed in 18 consecutive patients undergoing SLT early (24 to 72 hours), and in 10 of them late (3 to 6 months) after surgery. Right and left pulmonary vein flow were calculated as Qnu=A. VTI, where A, the pulmonary vein area, was derived as pi.(D/2)(2) and VTI is the velocity time integral of the pulmonary vein spectral display. Lung flow differential was calculated as the ratio of right (RQnu) or left (LQnu) pulmonary vein flow to total pulmonary venous flow (RQnu + LQnu). Lung perfusion imaging scintigraphy (technetium-99m) was used for comparison. Pulmonary vein velocity time integral of transplanted lung was significantly greater than that of native lung (34 +/- 9 vs 18 +/- 8 cm, p <0.001). Percent differential lung flow derived by perfusion imaging scintigraphy and by TEE showed a good correlation (r = 0.67, p <0.001). Pulmonary artery anastomoses were seen in all 12 right-lung recipients, and in 4 of the 6 left-lung recipients; no significant stenosis was noted in the arteries visualized. The pulmonary venous anastomoses were imaged in all patients. Small, nonocclusive pulmonary vein thrombi were seen in 1 patient. In conclusion, TEE is a useful method for calculating lung flow differential in patients undergoing SLT. In addition, TEE provides superb direct visualization of the venous and arterial anastomoses in most patients. Contrary to previous reports, the overall incidence of anastomotic complications is relatively low.

Gender differences in systolic left ventricular function in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).

Echocardiography was performed in 944 untreated hypertensive patients (391 women and 553 men, mean age 66 years) who had electrocardiographic left ventricular (LV) hypertrophy at baseline in the Losartan Intervention For End point reduction in hypertension (LIFE) study to evaluate gender-associated differences in systolic LV function. Women had significantly lower diastolic blood pressure (175/97 vs 173/99 mm Hg) and body surface area and a higher body mass index (all p < 0.01). Women also had higher LV ejection fraction (EF), endocardial and midwall fractional shortening (63% vs 60%, 35% and 33%, and 16% vs 15%, respectively, all p < 0.01), higher stress-corrected midwall fractional shortening (98% vs 96%, p < 0.05), and lower circumferential end-systolic wall stress (178 vs 187 kdynes/cm(2), p < 0.01). There was no difference in age or LV mass indexed for height(2.7), but relative wall thickness was higher in women (0.42 vs 0.41, p < 0.05). In multiple regression analyses: (1) EF and endocardial fractional shortening were 2% to 3% higher in women than men, independent of the effects of LV stress, body mass index, and height (multiple r = 0.77 and 0.75, respectively, gender p < 0.02 in both models); (2) midwall fractional shortening was 0.5% higher in women, independent of the effects of age, body mass index, circumferential end-systolic stress, and absence of diabetes (multiple r = 0.36, p = 0.014 for gender); and (3) stress-corrected LV midwall fractional shortening was 2% higher (p = 0.004) in women, independent of the effects of age, height, heart rate, body mass index, and diabetes (multiple r = 0.33). Thus, female gender is an independent predictor of higher systolic LV function in hypertensive patients with electrocardiographic LV hypertrophy.

Prevalence of diastolic dysfunction in normotensive, asymptomatic patients with well-controlled type 2 diabetes mellitus.

To evaluate the prevalence of left ventricular (LV) diastolic dysfunction in patients with type 2 diabetes mellitus free of cardiovascular disease, we studied 86 normotensive men and women (mean age 46 +/- 6 years) with Doppler echocardiography. All subjects were asymptomatic for ischemic heart disease or heart failure. The traditional transmitral filling patterns were used to characterize diastolic physiology. The Valsalva maneuver was used to differentiate normal from pseudonormal LV filling pattern. All patients had a normal electrocardiogram at rest and a negative result on exercise echocardiography for inducible wall motion abnormalities. Global LV systolic function was normal (mean LV ejection fraction 58%, range 53% to 76%). Diastolic dysfunction was found in 41 subjects (47%) of which 26 (30%) had impaired relaxation and 15 (17%) had a pseudonormal filling pattern. The mean LV mass index was 101 g/m2 (range 86 to 122). All patients with a normal-filling physiology had gender-adjusted normal LV mass index (mean 93 +/- 11 g/m2), whereas 62% of those with either abnormal relaxation (mean 103 +/- 12 g/m2, p <0.001) or a pseudonormal pattern (mean 110 +/- 12 g/m2, p <0.001) had increased LV mass index. No subject in this cohort had restrictive diastolic physiology. In conclusion, diastolic dysfunction in type 2 diabetes mellitus patients is often found despite adequate metabolic control and freedom from clinically detectable heart disease. The Valsalva maneuver can unmask an additional 17% of patients with subclinical abnormal LV filling pattern, who otherwise would be classified as having a normal diastolic physiology. Increased LV mass index is closely associated with abnormal LV filling characteristics.

Diagnostic and prognostic use of stress echo in acute coronary syndromes including emergency department imaging.

Early treatment of acute myocardial infarction (AMI) can improve the rate of coronary patency, salvage myocardium, and ultimately save lives; thus, rapid recognition of patients at a higher risk of developing AMI is very important. The clinical history in patients with documented AMI is sometimes atypical, and the initial cardiac enzyme levels often are within the normal range. Moreover, the typical ST-segment elevation is often absent on the initial electrocardiogram in patients who subsequently sustain an AMI. Stress-induced segmental wall motion abnormalities (SWMAs) in coronary artery disease patients can be readily detected by conventional two-dimensional echocardiography. Moreover, echocardiography is the only technique available that allows real-time assessment of stress-induced reduction in systolic wall thickening, a highly specific sign of myocardial ischemia. Echocardiography for the diagnosis of acute ischemia is most helpful in subjects with a high clinical suspicion but nondiagnostic electrocardiograms. Under these circumstances, reversible SWMA confirms the diagnosis of acute coronary syndrome. The location of regional SWMAs correlates well with the distribution of the artery involved and pathological evidence of infarction. A trained eye can easily recognize cardiac causes of acute chest pain other than coronary diseases such as aortic stenosis, hypertrophic cardiomyopathy, mitral valve prolapse, pericarditis, and aortic dissection. When echocardiography is performed soon after the patients arrival at the emergency department (ED) or during a chest pain episode, SWMAs are detected in 90-95% of transmural infarctions and in 80-90% of nontransmural or subendocardial infarctions, and the specificity of echocardiography is approximately 80-90%. Although stress echocardiography performed in the ED and interpreted at a distance through the use of telemedicine has the potential of being convenient, in our opinion, any form of stress echocardiography should be performed in the echocardiography laboratory only after an AMI has been completely ruled out. The detection of jeopardized myocardium early after AMI can identify patients at a higher risk to develop subsequent events. In conclusion, echocardiography is cost effective in the triage of patients presenting with acute chest pain when performed soon after ED admission or during a chest pain episode. However, echocardiography must be readily available, expeditiously performed, and skillfully interpreted. The clinical use of stress echocardiography in acute coronary syndromes has been greatly improved with the introduction of digital and second harmonics technology and further enhanced by the availability of contrast agents.

Pathophysiologic correlates of thromboembolism in nonvalvular atrial fibrillation: I. Reduced flow velocity in the left atrial appendage (The Stroke Prevention in Atrial Fibrillation [SPAF-III] study).

Stroke associated with atrial fibrillation (AF) is mainly due to embolism of thrombus formed during stasis of blood in the left atrial appendage (LAA). Pathophysiologic correlates of appendage flow velocity as assessed by transesophageal echocardiography (TEE) in patients with AF have not been defined. To evaluate the hypothesis that reduced velocity is associated with spontaneous echocardiographic contrast and thrombus in the LAA and with clinical embolic events, we measured LAA flow velocity by TEE in 721 patients with nonvalvular AF entering the Stroke Prevention in Atrial Fibrillation (SPAF-III) study. Patient features, TEE findings, and subsequent cardioembolic events were correlated with velocity by multivariate analysis. Patients in AF during TEE displayed lower peak antegrade (emptying) flow velocity (Anu(p)) than those with intermittent AF in sinus rhythm during TEE (33 cm/s vs 61 cm/s, respectively, P <.0001). Anu(p) < 20 cm/s was associated with dense spontaneous echocardiographic contrast (P <.001), appendage thrombus (P <.01), and subsequent cardioembolic events (P <.01). Independent predictors of Anu(p) < 20 cm/s included age (P =.009), systolic blood pressure (P <.001), sustained AF (P =.01), ischemic heart disease (P =.01), and left atrial area (P =.04). Multivariate analysis found both Anu(p) <20 cm/s (relative risk 2.6, P =.02) and clinical risk factors (relative risk 3.3, P =.002) independently associated with LAA thrombus. LAA Anu(p) is reduced in AF and associated with spontaneous echocardiographic contrast, appendage thrombus, and cardioembolic stroke. Systolic hypertension and aortic atherosclerosis, independent clinical predictors of stroke in patients with AF, also correlated with LAA Anu(p). Our results support the role of reduced LAA Anu(p) in the generation of stasis, thrombus formation, and embolism in patients with AF, although other mechanisms also contribute to stroke.

Pathophysiologic correlates of thromboembolism in nonvalvular atrial fibrillation: II. Dense spontaneous echocardiographic contrast (The Stroke Prevention in Atrial Fibrillation [SPAF-III] study).

We analyzed transesophageal echocardiograms from 772 participants in the Stroke Prevention in Atrial Fibrillation (SPAF-III) study, characterizing spontaneous echocardiographic contrast (SEC) in the left atrium or appendage as faint or dense. The association of dense SEC with stroke risk factors and anatomic, hemodynamic, and hemostatic parameters related to specific thromboembolic mechanisms was evaluated by multivariate analysis. Spontaneous echocardiographic contrast was present in 55% of patients and was dense in 13%. Age (odds ratio [OR] 2.4/decade, P <.001), constant atrial fibrillation (OR 6.9, P <.001), history of hypertension (OR 3. 2, P <.001), and current tobacco smoking (OR 2.6, P =.04) were independent clinical predictors of dense SEC. Multivariate analysis of clinical, echocardiographic, and hemostatic parameters yielded age as the sole independent clinical predictor of dense SEC (OR 2. 4/decade, P <.001). Other independent predictors were measures of left atrial/appendage flow dynamics, left atrial size (OR 2.4/cm diameter, M-mode, P <.001), atherosclerotic aortic plaque (OR 2.8, P =.002), and plasma fibrinogen >350 mg/dL (P <.001). Results were similar when SEC of any density was analyzed. In conclusion, SEC occurred in more than half of these patients with prospectively defined nonvalvular atrial fibrillation but was usually faint. Dense SEC was strongly associated with previously reported clinical predictors of stroke, linking them to thromboembolism through atrial stasis. Diverse pathophysiologic factors including atrial stasis, fibrinogen level, and aortic plaque influence SEC.

Aortic plaque in atrial fibrillation: prevalence, predictors, and thromboembolic implications.

BACKGROUND AND PURPOSE: Thoracic aortic plaque identified by transesophageal echocardiography heightens the risk of stroke associated with atrial fibrillation (AF). We sought to identify the prevalence, predictors, and implications of aortic plaque in patients with nonvalvular AF. METHODS: Thoracic aortic plaque was prospectively sought in 770 persons with AF with the use of transesophageal echocardiography and classified as simple or complex on the basis of thickness >/=4 mm, ulceration, or mobility. Clinical and echocardiographic features of thromboembolism were correlated by multivariate analysis. RESULTS: Aortic plaque was detected in 57% of the cohort, and complex plaque was detected in 25%. Both were found more frequently in the descending than in the proximal aorta. Potentially etiologic patient characteristics independently associated with complex plaque included advanced age, history of hypertension, diabetes, and past or present tobacco use. Comorbidities associated with aortic plaque were prior thromboembolism, increased pulse pressure, ischemic heart disease, stenosis or sclerosis of the aortic valve, mitral annular calcification (>10%), elevated serum creatinine concentration, spontaneous echo contrast in the left atrium or appendage, and left atrial appendage thrombus. The prevalence of complex plaque in patients aged <70 years with <10% mitral annular calcification, without ischemic heart disease, or without pulse pressure >/=65 mm Hg was 4% (95% CI, 1% to 6%). CONCLUSIONS: Aortic plaque is prevalent in patients with AF and is associated with atherosclerosis risk factors and with left atrial stasis or thrombosis, which are themselves independent stroke risk factors. Since the predominant location of complex plaque was in the descending aorta, the role of aortic plaque as a source of embolism in AF is uncertain.

Warfarin safety and efficacy in patients with thoracic aortic plaque and atrial fibrillation. SPAF TEE Investigators. Stroke Prevention and Atrial Fibrillation. Transesophageal echocardiography.

Patients with atrial fibrillation and with documented aortic plaque who were assigned to adjusted-dose warfarin therapy (international normalized ratio 2.0 to 3.0) had an annual rate of cholesterol embolization of 0.7% (95% confidence interval [CI] 0.1% to 5.3%/patient-year). Warfarin-assigned patients with plaque had a lower rate of embolic events (5.9%/year; 95% CI 3.0 to 12) than those on combination low-dose warfarin (international normalized ratio <1.5) plus aspirin (17.3%/year; 95% CI 11 to 27; p = 0.01).

Left atrial diameter in nonvalvular atrial fibrillation: An echocardiographic study. Stroke Prevention in Atrial Fibrillation Investigators.

BACKGROUND: The left atrium (LA) is usually enlarged in patients with nonvalvular atrial fibrillation (AF), but factors associated with LA diameter are incompletely defined. METHODS AND RESULTS: This transthoracic echocardiographic cohort study includes 3465 participants with nonvalvular AF in 3 multicenter clinical trials. LA diameter determined by M-mode echocardiography was correlated with clinical and echocardiographic features by cross-sectional multivariate regression analyses. The mean LA diameter was 47 +/- 8 mm, on average 6 mm larger in those with AF at the time of echocardiography than in those with sinus rhythm (48 vs 42 mm, P <. 001). Patient age and body weight were independently predictive of LA diameter (P <.0001), but sex, body surface area, and body mass index were not. The estimated independent contribution of atrial rhythm to LA diameter was approximately 2.5 mm. Prolonged duration of AF, left ventricular dilatation and increased muscle mass, mitral regurgitation, annular calcification, and hypertension were additional independent predictors of LA diameter. CONCLUSIONS: Multiple factors appear to contribute to LA enlargement in patients with nonvalvular AF, including the presence and persistence of the dysrhythmia.

Comparison in systemic hypertension of left ventricular mass and geometry with systolic and diastolic function in patients <65 to > or = 65 years of age.

Previous studies have differed on the independent effect of age and gender to left ventricular (LV) mass. Data on ventricular remodeling in hypertensive patients > or = 65 years of age is lacking. Similarly, the systolic and diastolic interaction in older hypertensives is not well defined. In a prospective study, we examined the relation of LV mass, relative wall thickness, and systolic and diastolic interaction in 508 hypertensive patients between 50 and 80 years of age who were divided according to age (<65 and > or = 65 years) and gender. LV mass, geometric classification, systolic wall stress, and Doppler filling were obtained according to standard Doppler echocardiographic criteria. In men, most measurements were similarly distributed. However, women > or = 65 years of age had smaller LV systolic dimensions, thicker ventricular septums, higher endocardial and midwall fractional shortenings, and lower end-systolic wall stress. Although LV mass was higher in men, there was no age difference within the same sex. The most common LV geometric remodeling was increased relative wall thickness in the form of concentric hypertrophy or concentric remodeled. The predominant mitral flow pattern was "impaired relaxation"; however, older patients had even shorter E waves, taller A waves, and lower E/A ratios. Thus, patients > or = 65 years of age had an even higher prevalence of this pattern (men, 89% vs 73%, p <0.001, and women, 91% vs 77%, p <0.001). Delayed LV relaxation with preservation of systolic ejection indexes is an early abnormality in essential hypertension, which lasts an undetermined time with further progression as patients aged. As a result, hypertensive patients > or = 65 years of age had the most pronounced structural and functional changes, an observation particularly noted in women. In those > or = 65 years, data from the Doppler E wave and A wave do not distinguish the physiologic process of aging from the pathologic changes of pressure overload.

Transesophageal echocardiographic correlates of clinical risk of thromboembolism in nonvalvular atrial fibrillation. Stroke Prevention in Atrial Fibrillation III Investigators.

OBJECTIVES: This study explored the mechanisms linking clinical and precordial echocardiographic predictors to thromboembolism in atrial fibrillation (AF) by assessing transesophageal echocardiographic (TEE) correlations. BACKGROUND: Clinical predictors of thromboembolism in patients with nonvalvular AF have been identified, but their mechanistic links remain unclear. TEE provides imaging of the left atrium, its appendage and the proximal thoracic aorta, potentially clarifying stroke mechanisms in patients with AF. METHODS: Cross-sectional analysis of TEE features correlated with low, moderate and high thromboembolic risk during aspirin therapy among 786 participants undergoing TEE on entry into the Stroke Prevention in Atrial Fibrillation III trial. RESULTS: TEE features independently associated with increased thromboembolic risk were appendage thrombi (relative risk [RR] 2.5, p = 0.04), dense spontaneous echo contrast (RR 3.7, p < 0.001), left atrial appendage peak flow velocities < or = 20 cm/s (RR 1.7, p = 0.008) and complex aortic plaque (RR 2.1, p < 0.001). Patients with AF with a history of hypertension (conferring moderate risk) more frequently had atrial appendage thrombi (RR 2.6, p < 0.001) and reduced flow velocity (RR 1.8, p = 0.003) than low risk patients. Among low risk patients, those with intermittent AF had similar TEE features to those with constant AF. CONCLUSIONS: TEE findings indicative of atrial stasis or thrombosis and of aortic atheroma were independently associated with high thromboembolic risk in patients with AF. The increased stroke risk associated with a history of hypertension in AF appears to be mediated primarily through left atrial stasis and thrombi. The presence of complex aortic plaque distinguished patients with AF at high risk from those at moderate risk of thromboembolism.

Hypertension optimal treatment (HOT) study: home blood pressure in treated hypertensive subjects.

The Hypertension Optimal Treatment Study is a prospective trial conducted in 26 countries. The aims are to (1) evaluate the relationship between three levels of target office diastolic blood pressure (BP) (< or = 80, < or = 85, or < or = 90 mm Hg) and cardiovascular morbidity and mortality in hypertensive patients and (2) examine the effects on cardiovascular morbidity and mortality of 75 mg aspirin daily versus placebo. A total of 19,193 patients between 50 and 80 years of age had been randomized by the end of April 1994. Treatment was initiated with felodipine 5 mg daily, and additional therapy was given in accordance with a set protocol. The present substudy of 926 patients performed in nine countries aimed to (1) compare home with office BP in a representative subsample of the HOT population after the titration of treatment was completed and (2) clarify whether the separation into the target groups could be expanded into the out-of-office setting. The differences between office and home measurements in diastolic BP of 0.2 mm Hg (SD, 9; 95% confidence interval, -0.36 to 0.81; P=.40) and systolic BP of 0.5 mm Hg (SD, 15; 95% confidence interval, -0.53 to 1.46; P=.21) were not significant. The group differences in home BP were 1.9 mm Hg (< or = 80 versus < or = 85) and 1.2 mm Hg (< or = 85 versus < or = 90) for diastolic BP (F=11.69; ANOVA, P<.0001) and 2.6 and 2.1 mm Hg for systolic BP (F=8.44, P=.0002). Thus, office and home BPs measured with the same semiautomatic device are comparable in treated hypertensive subjects in the HOT Study, and the separation into the target groups based on office readings prevails at home.

Variation of flow propagation velocity with age.

Flow propagation velocity is a new color Doppler M-mode measurement of left ventricular filling characteristics. This study was designed to establish normal values for this measurement in healthy individuals and to compare these findings with pulsed Doppler transmitral velocities. Complete M-mode, two-dimensional, and Doppler echocardiographic studies were performed on 64 volunteers between 21 and 79 years of age. Significant negative correlations (p < 0.001) with age were noted for flow propagation velocity (r = -0.59), peak early diastolic filling velocity (r = -0.65), and peak early diastolic filling/peak atrial filling ratio (r = -0.80). Positive correlations (p < 0.001) with age were observed for peak atrial filling velocity (r = 0.50) and atrial filling velocity integral (r = 0.71). Flow propagation velocity decreased by 44% between the youngest and oldest age groups. We conclude that flow propagation velocity is influenced by age and that it compares favorably with transmitral Doppler indices of left ventricular filling in this regard. These age-related alterations are present in healthy individuals, in the absence of any apparent cardiovascular disease.

Impact of ethnicity on left ventricular mass and relative wall thickness in essential hypertension.

This study was designed to evaluate the impact of ethnicity on left ventricular (LV) mass, and relative wall thickness in 527 patients (57% men, mean age 60 +/- 7 years) with mild to moderate high blood pressure. There were 63% Caucasians, 21% African-Americans, and 16% Hispanics. LV mass was indexed according to body surface area, height, and height to the allometric power of 2.7. Relative wall thickness included the 4 widely recognized patterns: normal, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy. LV mass indexed to body surface area was similar among all 3 ethnic groups (Caucasians 117.1 g/m2, African-Americans 119.2 g/m2, Hispanics 122.7 g/m2); however, when indexed to height and height to the power of 2.7, Hispanics had slightly larger masses than the other 2 groups (Hispanics 168.1 and 73.3 g/m2.7 vs Caucasians 159.8 and 64.4 g/m2.7 [p = NS and p < 0.005]; and vs African-Americans 164.8 and 69.2 g/m2.7 [p = NS for both]). Using body surface area, the concentric remodeling was the predominant form of cardiac adaptation in Caucasians (36%) and African-Americans (42%), whereas the concentric hypertrophy pattern was 38% in Hispanics. Using indexing for both height and height to the power of 2.7, the concentric hypertrophy pattern predominated in all 3 ethnic groups (Caucasians 48% and 51%; African-Americans 68% and 66%; Hispanics 59% and 65%). In conclusion, because of the independent impact of weight on high blood pressure, LV mass adjusted to height or to height at the power of 2.7 should be reported in population studies. The concentric hypertrophy pattern--classic LV response to pressure overload conditions--is better represented when LV mass is indexed to height or to height to the allometric power of 2.7 than to body surface area.

Safety and efficacy of closed-loop arbutamine stress echocardiography for detection of coronary artery disease. International Arbutamine Study Group.

Closed-loop arbutamine stress echocardiography has been shown to be safe and effective for detecting coronary artery disease (CAD) using a standardized infusion protocol and centralized core laboratory analyses. However, the accuracy of arbutamine stress echocardiography using local test interpretation has not been previously tested in a large population. The present study reports the safety, sensitivity, and specificity of arbutamine stress echocardiography in a multicenter trial allowing user-defined, nonstandardized protocols and local test interpretation. In all, 1,070 patients underwent arbutamine stress testing at 81 sites. Heart rate increased from 73 +/- 13 to 124 +/- 15 beats/min, systolic blood pressure from 144 +/- 24 to 174 +/- 25 mm Hg, and pressure rate product x 10(3) from 10.5 +/- 2.8 to 19.6 +/- 3.9. Among 1,070 patients, there were only 2 (0.2%) significant adverse events related to arbutamine, both of which resolved completely with appropriate therapy. There were no incidents of ventricular fibrillation, sustained ventricular tachycardia, or death related to testing. Among 242 patients who underwent arbutamine stress echocardiography and diagnostic coronary angiography within 12 weeks, sensitivity and specificity for detection of CAD were 71% (95% confidence interval 64% to 77%) and 67% (95% confidence interval 52% to 80%), respectively. Closed-loop arbutamine stress echocardiography is a safe and effective method for evaluating CAD in clinical practice.