Frequency, characteristics, and outcome of patients with aortic stenosis, left ventricular dysfunction, and high (versus low) trans-aortic pressure gradient.

BACKGROUND: Trans-aortic pressure gradient in patients with aortic stenosis and left ventricular systolic dysfunction is typically low but occasionally high. OBJECTIVES: To examine the distribution of trans-aortic PG in patients with severe AS and severe LV dysfunction and compare the clinical and echocardiographic characteristics and outcome of patients with high versus low PG. METHODS: Using the echocardiographic laboratory database at our institution, 72 patients with severe AS (aortic valve area < or = 1.0 cm2) and severe LV dysfunction (LV ejection fraction < or = 30%) were identified. The characteristics and outcome of these patients were compared. RESULTS: PG was high (mean PG > or = 35 mmHg) in 32 patients (44.4%) and low (< 35 mmHg) in 40 (55.6%). Aortic valve area was slightly smaller in patients with high PG (0.63 + 0.15 vs. 0.75 +/- 0.16 cm2 in patients with low PG, P = 0.003), and LV ejection fraction was slightly higher in patients with high PG (26 +/- 5 vs. 22 +/- 5% in patients with low PG, P = 0.005). During a median follow-up period of 9 months 14 patients (19%) underwent aortic valve replacement and 46 patients (64%) died. Aortic valve replacement was associated with lower mortality (age and gender-adjusted hazard ratio 0.19, 95% confidence interval 0.05-0.82), whereas trans-aortic PG was not (P = 0.41). CONCLUSIONS: A large proportion of patients with severe AS have relatively high trans-aortic PG despite severe LV dysfunction, a finding partially related to more severe AS and better LV function. Trans-aortic PG is not related to outcome in these patients.

Functional tricuspid regurgitation in patients with pulmonary hypertension: is pulmonary artery pressure the only determinant of regurgitation severity?

BACKGROUND: Pulmonary hypertension is a common cause of functional tricuspid regurgitation (TR), but other factors play a role in determining TR severity. The objectives of our study were to determine the distribution of TR severity in relation to pulmonary artery systolic pressure (PASP) and to define the determinants of TR severity. METHODS: The echocardiographic reports and selected echocardiographic studies of patients with echocardiographic estimation of PASP were reviewed. Patients with organic tricuspid valve (TV) disease were excluded from the analysis. RESULTS: Among 2,139 patients, the frequency of moderate or severe TR was progressively greater in patients with higher PASP. Nevertheless, TR was only mild in a substantial proportion of patients with high PASP (mild TR in 65.4% of patients with PASP 50-69 mm Hg and in 45.6% of patients with PASP >or= 70 mm Hg). By multivariate analysis, age, female gender, PASP (odds ratio, 2.26 per 10-mm Hg increase; 95% confidence interval, 1.95 to 2.61), pacemaker lead, right atrial (RA) and right ventricular enlargement, left atrial enlargement, and organic mitral valve disease were independently associated with greater degrees of TR. In patients with PASP >or= 70 mm Hg, RA size, tricuspid annular diameter, and TV tethering area were greater in patients with greater degrees of TR. CONCLUSIONS: PASP is a strong determinant of TR severity, but many patients with pulmonary hypertension do not exhibit significant TR. In addition to PASP, demographic characteristics, mechanical factors, remodeling of the right heart cavities, and other factors (possibly reflecting the presence of atrial fibrillation or occult organic TV disease) are predictive of TR severity.

Relation of statin therapy to risk of heart failure after acute myocardial infarction.

Recent studies suggest that statin therapy reduces hospitalizations for heart failure (HF). However, few data exist regarding the role of statins in preventing HF after acute myocardial infarction (AMI). In addition, the potential impact of left ventricular (LV) ejection fraction (EF) and coexisting functional mitral regurgitation (MR) on the efficacy of statin therapy was not considered. We prospectively studied 1,563 patients with AMI. The primary endpoint was readmission for the treatment of HF. The effect of statin therapy initiated before hospital discharge was evaluated using a Cox model, adjusting for clinical variables, a propensity score for statin therapy, LVEF, and MR grade. Patients with recurrent infarctions were censored. Statins were prescribed in 1,048 patients (67.1%) before hospital discharge. During a median follow-up of 17 months, admissions for HF were lower in patients receiving statins (6.5% vs 14.8%; unadjusted hazard ratio 0.45, 95% confidence interval 0.32 to 0.63, p <0.0001). In a multivariable Cox model, statin therapy was associated with a significant reduction of hospitalization for HF (HR 0.62, 95% confidence interval 0.43 to 0.89, p = 0.009). There was a significant interaction between MR and statin therapy (p = 0.039), such that the beneficial effect of statins on HF hospitalizations was most pronounced in patients without concomitant MR and absent in patients with hemodynamically significant MR. In conclusion, in patients with AMI statin therapy initiated before hospital discharge significantly reduces subsequent hospitalizations for HF. The effect of statins is driven largely by the reduction in events in patients without concomitant hemodynamically significant MR.

Echocardiography-based spectrum of severe tricuspid regurgitation: the frequency of apparently idiopathic tricuspid regurgitation.

BACKGROUND: The cause of tricuspid valve (TV) regurgitation (TR) occasionally remains unclear. The objectives of our study were to define the causal spectrum of severe TR diagnosed by echocardiography at a tertiary medical center and to assess the relative frequency and determine the clinical and echocardiographic characteristics of TR without an apparent cause (idiopathic TR). METHODS: Consecutive patients with severe TR were identified by the echocardiography laboratory computerized database. The echocardiographic reports of all patients were reviewed and the causes of TR were determined. The echocardiographic studies and medical charts were reviewed in patients without an obvious cause of TR. RESULTS: Of 242 consecutive patients diagnosed with severe TR, organic TV disease was evident in 23 patients (9.5%) and significant pulmonary hypertension (estimated pulmonary artery systolic pressure > 50 mm Hg) in an additional 157 patients (64.9%). After further excluding patients with various confounding factors, possibly associated with occult organic TV disease or significant pulmonary hypertension, 23 patients (9.5%) had severe TR without an apparent cause. Of these, TV coaptation appeared relatively intact, allowing adequate estimation of pulmonary artery pressure, in 15 patients (6.2% of all patients with severe TR; idiopathic TR group). Patients with idiopathic TR were older (76 +/- 10 years), with a high frequency of atrial fibrillation (93%), and prominent TV annular dilatation. CONCLUSIONS: After excluding multiple potential causes of TR, severe TR is occasionally idiopathic. Annular dilatation (secondary to aging, atrial fibrillation, or other causes) is the likely mechanism of TR in these patients.

Ischemic mitral regurgitation and risk of heart failure after myocardial infarction.

BACKGROUND: The development of ischemic mitral regurgitation (MR) after myocardial infarction may impose hemodynamic load during a period of active left ventricular remodeling and promote heart failure (HF). However, few data are available on the relationship between ischemic MR and the long-term risk for HF. METHODS: We prospectively studied 1190 patients admitted for acute myocardial infarction. Mitral regurgitation was assessed by echocardiography and was considered mild, moderate, and severe when the regurgitant jet area occupied less than 20%, 20% to 40%, and greater than 40% of the left atrial area, respectively. The median duration of follow-up was 24 months (range, 6-48 months). RESULTS: Mild and moderate or severe ischemic MR was present in 39.7% and 6.3% of patients, respectively. After adjusting for ejection fraction and clinical variables (age, sex, Killip class, previous infarction, hypertension, diabetes mellitus, anterior infarction, ST-elevation infarction, and coronary revascularization), compared with patients without MR, the hazard ratios for HF were 2.8 (95% confidence interval [CI], 1.8-4.2; P<.001) and 3.6 (95% CI, 2.0-6.4; P<.001) in patients with mild and moderate or severe ischemic MR, respectively. The adjusted hazard ratios for death were 1.2 (95% CI, 0.8-1.8; P = .43) and 2.0 (95% CI, 1.2-3.4; P = .02) in patients with mild and moderate or severe MR, respectively. CONCLUSIONS: There is a graded independent association between the severity of ischemic MR and the development of HF after myocardial infarction. Even mild ischemic MR is associated with an increase in the risk of HF.

Left ventricular filling hemodynamics in patients with pulmonary edema and preserved versus reduced left ventricular ejection fraction: a prospective Doppler echocardiographic study.

BACKGROUND: Objective evidence of elevated left ventricular (LV) filling pressures is infrequently demonstrated in clinical practice in patients with heart failure (HF) and preserved LV ejection fraction (LVEF) and the clinical diagnosis of HF is commonly questionable in these patients. The objective of this study was to examine whether elevated LV filling pressures can be demonstrated noninvasively in consecutive patients with HF and preserved (vs reduced) LVEF. METHODS: Echocardiography was performed in 141 patients hospitalized with acute pulmonary edema (within 3 days of admission in 83.6%). LV filling was assessed in 116 patients without significant valve disease (median age 76 years; 51.7% men) and LV filling pressures were estimated based on mitral and pulmonary venous flow patterns and mitral annular diastolic velocities. RESULTS: LVEF was preserved (> or =45%) in 49 patients (42.2%) and reduced (<45%) in 67 patients (57.8%). In patients with in sinus rhythm, normal LV filling pattern and abnormal relaxation, pseudonormal, and restrictive LV filling patterns (the latter two patterns associated with elevated LV filling pressures) were evident in 8, 1, 11, and 9 patients with preserved LVEF, versus 5, 11, 15, and 23 patients with reduced LVEF, respectively (P = .01) (LV filling pattern was nonconclusive in 12 patients). In patients with atrial arrhythmias, elevated LV filling pressures were evident in 4 of 14 patients with preserved LVEF and 3 of 4 patients with reduced LVEF. Overall, elevated LV filling pressures were demonstrable in 24 patients with preserved LVEF (49.0%) and in 41 patients with reduced LVEF (68.3%) (P = .26). CONCLUSIONS: Elevated LV filling pressures are frequently evident by Doppler echocardiography in patients with HF and preserved or reduced LVEF. Thus, Doppler echocardiography can provide objective noninvasive evidence of abnormal LV filling in a large proportion of patients with HF and preserved LVEF.

Intermittent coronary sinus occlusion complicating coronary sinus cannulation during coronary artery bypass operation.

Coronary sinus (CS) thrombosis is a rare event, usually complicating invasive procedures that cause trauma to the CS. Based on anecdotal case reports, this pathology is frequently associated with serious complications and is commonly fatal. We describe a case of intermittent CS thrombosis resulting from CS cannulation during coronary artery bypass grafting operation. This complication was further complicated by myocardial infarction, left ventricular free wall rupture, and pseudoaneurysm formation. The characteristic echocardiographic findings and a review of the literature on this rare complication are presented.

Pericardiocentesis ending in the superior vena cava.

Pericardiocentesis is associated with a wide range of complications. We describe a pericardiocentesis attempt ending in the superior vena cava through the route of liver parenchyma, hepatic vein, inferior vena cava, and right atrium.