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Objectives The purpose of this study was to investigate the cause of abnormal left ventricular (LV) Doppler diastolic filling characteristics in chronic thromboembolic pulmonary hypertension (CTEPH). Background In CTEPH, LV diastolic function often appears abnormal. It is unclear whether this “impaired relaxation” (E Methods We studied 61 patients with an E Results After PTE, mitral E velocity increased (from 54 ± 16 cm/s to 81 ± 20 cm/s, p m ) did not change after PTE (8.0 ± 3.1 cm/s to 8.1 ± 2.0 cm/s, p = ns), whereas the velocity of the lateral mitral annulus increased (9.3 ± 3.2 cm/s to 11.8 ± 3.1 cm/s, p Conclusions The results of this study strongly suggest that the impaired relaxation pattern observed in patients with CTEPH is not solely the result of geometric effects of RV enlargement and LV chamber distortion but is caused in large part by low LV preload and relative underfilling.

The cellular mechanisms following myocardial infarction remain poorly characterized. It is believed that an inflammatory and immunologic process may be involved and that the beneficial effects of enalapril on remodeling may, in part, work through an immune mechanism. To characterize the effect of enalapril on immune alterations in the late phase of ventricular remodeling after myocardial infarction, rats underwent left coronary artery ligation followed by 6 weeks of either enalapril or placebo treatment. Infarct sizes, heart weights, and volumes were compared. Peripheral and splenic leukocyte and lymphocyte subsets, along with T cell blastogenesis, were quantified in enalapril treated rats 6 weeks after coronary ligation and compared to untreated control rats. Additionally, antibody production to a de novo antigen, keyhole limpet hemocyanin, was assessed with and without treatment. Average infarct size was equivalent among enalapril-treated myocardial infarction rats and untreated infarct rats. There was, however, less left and right ventricular hypertrophy in the enalapril treated group. Enalapril completely prevented the 42% increase in white blood count, the 88% increase in neutrophils, and the 28% increase in lymphocyte count seen in untreated infarct rats. Both untreated and enalapril treated rats tended toward a decrease in T helper:suppressor ratio. All rats treated with enalapril, however, had a significant increase in the T helper:suppressor ratio versus untreated control rats (F = 3.6, P = .018). Blastogenesis was markedly increased in T cells from infarcted animals. This was mitigated by treatment with enalapril. Additionally, immunoglobulin G antibody production was significantly lessened in rats treated with enalapril. The results of this study suggest that alterations in immunoregulatory cell type and function occurs following myocardial infarction. The beneficial effects of the angiotensin-converting enzyme inhibitor enalapril may be, in part, due to its mitigating effects on immune cell release and activation following myocardial infarction.

Studies have shown that left ventricular cardiac power output (CPO) is a measure of global cardiac function and a predictor of cardiogenic shock mortality. The utility of right ventricular (RV) CPO, however, is unclear. Our aim was to investigate RV CPO in patients with chronic thromboembolic

Transesophageal echocardiography continues to evolve as an important complimentary technique to transthoracic echocardiography for the diagnosis and management of various cardiovascular disorders. Improved transducer technology has expanded the indications to include assessment of ventricular function, especially in the intraoperative setting. Automatic border detection may further simplify the quantitative approach of transesophageal echocardiographic-guided assessment of ventricular function. Another area in which the technique continues to develop is valvular disease, especially for planimetry of the aortic valve area in aortic stenosis. The technique continues to be used in the evaluation of endocarditis, especially prosthetic valve involvement, and for the evaluation of the patient with a potential cardiac source of emboli. Clearly, transesophageal echocardiography plays an important role in evaluating lesions of the aorta, particularly dissection, where it may be the diagnostic test of choice. Undoubtedly, the technique will continue to evolve with changes driven by developments in technology.

Background Echocardiographic evaluation of left ventricular (LV) strain and strain rate (SR) by 2D speckle tracking may be useful tools to assess chronic thromboembolic pulmonary hypertension (CTEPH) severity as well as response to successful pulmonary thromboendarterectomy (PTE). Methods We evaluated 30 patients with CTEPH before and after PTE using 2D speckle tracking measurements of LV radial and circumferential strain and SR in the short axis, and correlated the data with right heart catheterization (RHC). Results PTE resulted in a decrease in mean PA pressure (44 ± 15 to 29 ± 9 mmHg), decrease in PVR (950 ± 550 to 31 ± 160 [dyne-sec]/cm5), and an increase in cardiac output (3.9 ± 1.0 to 5.0 ± 1.0 L/min, p < 0.001 for all). Circumferential and posterior wall radial strain changed by -11% and +15% respectively (p < 0.001 for both). Circumferential SR and posterior wall radial SR changed by -7% and 6% after PTE. While the increase in posterior wall SR with PTE reached statistical significance (p = 0.04) circumferential SR did not (p = 0.07). In addition, septal radial strain and SR did not change significantly after PTE (p = 0.1 and 0.8 respectively). Linear regression analyses of circumferential and posterior wall radial strain and SR revealed little correlation between strain/SR measurements and PVR, mean PA pressure, or cardiac output. However, change in circumferential strain and change in posterior wall radial strain correlated moderately well with changes in PVR, mean PA pressure and cardiac output (r = 0.69, 0.76, and 0.51 for circumferential strain [p < 0.001 for all] and r = 0.7, 0.7, 0.45 for posterior wall radial strain [p = 0.001, 0.001, and 0.02, respectively]). Conclusions LV circumferential and posterior wall radial strain change after relief of pulmonary arterial obstruction in patients with CTEPH, and these improvements occur rapidly. These changes in LV strain may reflect effects from improved LV diastolic filling, and may be useful non-invasive markers of successful PTE.

The purpose of this study was to investigate the cause of abnormal left ventricular (LV) Doppler diastolic filling characteristics in chronic thromboembolic pulmonary hypertension (CTEPH).In CTEPH, LV diastolic function often appears abnormal. It is unclear whether this "impaired relaxation" (EA) filling pattern is caused by septal hypertrophy, right ventricular (RV) enlargement and LV chamber distortion, or low LV preload and underfilling.We studied 61 patients with an EA transmitral pattern and CTEPH who underwent pulmonary thromboendarterectomy (PTE). We compared the results of pre- and postoperative transthoracic echocardiography and right heart catheterization measurements.After PTE, mitral E velocity increased (from 54 +/- 16 cm/s to 81 +/- 20 cm/s, p0.001), whereas A velocity decreased (77 +/- 22 cm/s to 71 +/- 20 cm/s, p0.001). E/A ratio normalized (0.72 +/- 0.16 cm/s to 1.22 +/- 0.40 cm/s, p0.001). Pulmonary venous systolic and diastolic velocities both increased (57 +/- 13 cm/s to 68 +/- 16 cm/s and 39 +/- 15 cm/s to 70 +/- 21 cm/s, respectively, p0.001 for both). Diastolic velocity of the septal mitral annulus (E(m)) did not change after PTE (8.0 +/- 3.1 cm/s to 8.1 +/- 2.0 cm/s, p = ns), whereas the velocity of the lateral mitral annulus increased (9.3 +/- 3.2 cm/s to 11.8 +/- 3.1 cm/s, p0.001). Mean pulmonary capillary wedge pressure increased from 9.3 +/- 3.2 mm Hg to 10.6 +/- 3.8 mm Hg (p = 0.035). Despite these marked changes in LV inflow, M-mode measurements of LV septal and posterior wall thickness were normal before PTE and did not change after surgery (septal: 10 +/- 2 mm vs. 10 +/- 1 mm; posterior: 10 +/- 2 mm vs. 10 +/- 1 mm; p = NS for both comparisons).The results of this study strongly suggest that the impaired relaxation pattern observed in patients with CTEPH is not solely the result of geometric effects of RV enlargement and LV chamber distortion but is caused in large part by low LV preload and relative underfilling.

Pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) are important hemodynamic parameters in patients with advanced cardiopulmonary disease. We undertook this study to determine whether Doppler tissue imaging of the tricuspid annulus could be used to assess PAP and PVR noninvasively.We studied 50 consecutive patients with suspected chronic thromboembolic pulmonary hypertension referred to our center for evaluation. We performed preoperative transthoracic echocardiography with Doppler tissue imaging of the tricuspid annulus. All patients then underwent cardiac catheterization with invasive determination of cardiac output, PAP, and PVR.The systolic velocity of the tricuspid annulus (tS(m)) had an inverse relationship with catheterization-derived mean PAP, with a correlation coefficient of -0.493 (P = .0003). The inverse correlation of tS(m) with catheterization-derived PVR was more striking, with a correlation coefficient of -0.710 (P.0001). Based on the data, we derived the following logarithmic regression equation: PVR = 3698 - 1227 x ln(tS(m)).Doppler tissue imaging of the lateral tricuspid annulus is a useful clinical tool that can provide a noninvasive estimate of PVR in patients with chronic thromboembolic pulmonary hypertension. In this population, decreasing values of tS(m) predicted progressively higher measurements of PVR.

Common femoral artery stenosis is well appreciated in patients with peripheral arterial disease, but not described following repeated arterial access. We present a case of progressive right common femoral artery stenosis resulting in resting leg ischemia and ulceration that was temporally related to multiple ipsilateral vascular access procedures for recurrent coronary and peripheral diagnostic and therapeutic procedures. We hypothesize that recurrent arterial injury in a setting of diabetes resulted in progressive critical common femoral artery stenosis.

Doppler tissue imaging (DTI) of mitral annular velocity is useful in assessing diastolic function. Most centers record at the septal or lateral segments of the annulus. Cardiopulmonary bypass produces changes in the motion of the interventricular septum. We evaluated the use of DTI after operation with and without cardiopulmonary bypass. 18 patients scheduled for cardiac surgery were prospectively examined. Nine underwent cardiopulmonary bypass. Nine had operation without bypass. DTI was performed 4 +/- 3 days before operation and again 31+/- 7 days afterwards. Early diastolic velocities of the lateral and septal segments of the mitral annulus were measured. Ejection fraction and transmitral diastolic early-to-late filling (E/A) ratios were also assessed. Early diastolic septal mitral annular velocity decreased (7.9 +/- 1.2 to 5.9 +/- 1.1 cm/s [P= .001]) after on-pump operation whereas lateral segment velocity remained unchanged (8.5 +/- 2.9 to 8.2 +/- 3.7 cm/s [P = .30]). E/A ratio did not change after operation (1.28 +/- 0.25 to 1.21 +/- 0.47 [P = .45]). In contrast, septal segment velocity in the off-pump group trended higher after operation (5.3 +/- 1.9 to 6.0 +/- 1.5 cm/s [P = .20]). Lateral segment velocity and E/A ratio also increased somewhat, but changes were not significant (6.2 +/- 1.7 to 6.7 +/- 2.9 cm/s [P = .15] and 1.1 +/- 0.5 to 1.2 +/- 0.4 [P = .13], respectively). Ejection fraction increased in both groups. Early diastolic velocity of the septal mitral annulus decreases after operation with cardiopulmonary bypass, but does not change after off-pump operation. In contrast, early diastolic velocity of the lateral segment is not affected by either on-pump or off-pump operation. Measuring lateral segment velocity is recommended for diastolic DTI after cardiopulmonary bypass, as septal DTI may incorrectly suggest diastolic dysfunction.

Objectives. This study sought to characterize the effects of prolonged catecholamine infusion on immunoregulatory cell traffic and activation. Background. Immunoregulation has been shown to be partially controlled by the sympathetic nervous system. Although short-term elevation of catecholamine levels is known to alter immunoregulatory cell traffic and activation, the effects of prolonged heightened sympathetic nervous system activity have not adequately been studied. We believe that the alterations in immune function seen in patients with congestive heart failure are linked to a prolonged elevation of circulating catecholamine levels. Methods. To characterize the effects of prolonged elevation of catecholamine levels, rats received 4 weeks of constant infusion of epinephrine or norepinephrine through implanted osmotic minipumps. Peripheral and splenic leukocyte subsets, T cell proliferation and interleukin-2 receptor expression were quantified. Antibody production to the novel antigen keyhole limpet hemocyanin was assessed over the 4-week treatment period. Results. Both epinephrine and norepinephrine caused significant splenic atrophy and cardiac hypertrophy; both were blocked by propranolol. Epinephrine induced lymphocytosis; both cat, echolamines caused an increase in natural killer cells. In the spleen, both epinephrine and norepinephrine led to a dose-dependent decrease in total T cells, suppressor/cytotoxic T cells and natural killer cells and a significant increase in B cells. Epinephrine at the low dose enhanced mitogen-induced proliferation and interleukin-2 receptor expression. Norepinephrine at the low dose appeared to diminish proliferation. Epinephrine tended to inhibit IgG antibody production, whereas norepinephrine had no effect. Conclusions. The results of our study indicate that prolonged elevation of catecholamine levels alters immune cell proliferation and differentiation. These alterations differ greatly from those induced by short-term stimulation but, for the most part, parallel those found in patients with congestive heart failure. We postulate that the shifts in immunoregulatory cell type and function seen in patients with congestive heart failure are due, in part, to longstanding increases in circulating catecholamine levels and may play an important role in the pathogenesis and progression of disease.

ObjectivesWe evaluated the utility of tissue Doppler-derived right ventricular (RV) Tei (or myocardial performance) index in patients with chronic thromboembolic pulmonary hypertension (CTEPH) before and after pulmonary thromboendarterectomy (PTE) and assessed correlations with mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac output (CO).BackgroundThe assessment of RV function is limited with 2-dimensional echocardiography. The RV Tei index, an indicator of RV myocardial performance, is derived by Doppler measurements and is unaffected by RV geometry. The use of tissue Doppler imaging (at the lateral tricuspid annulus) for RV Tei index calculation is simple and eliminates the need for pulsed-wave Doppler recordings of both RV inflow and outflow.MethodsNinety-three patients with CTEPH were prospectively studied along with 13 control patients. Right ventricular tissue Doppler imaging and right heart catheterization were performed before and after PTE. Right ventricular Tei index was compared with values of mPAP, PVR, and CO with the use of linear regression.ResultsRight ventricular Tei index was 0.52 ± 0.19 in patients with CTEPH and 0.27 ± 0.09 in control patients (p < 0.0001). After PTE, RV Tei index decreased to 0.33 ± 0.10 (p < 0.0001). Pulmonary vascular resistance correlated well with RV Tei index before (r = 0.78, p < 0.0001) and after (r = 0.67, p < 0.0001) surgery. Also, the absolute change in Tei index in each patient after PTE correlated well with the concomitant change in PVR (r = 0.75, p < 0.0001). RV Tei index did not correlate as well with mPAP (pre-operatively: r = 0.55, p < 0.0001; post-operatively: r = 0.26, p = 0.03) or CO (pre-operatively: r = 0.57, p < 0.0001; post-operatively: r = 0.43, p < 0.0001).ConclusionsThese results demonstrate a correlation between RV Tei index and right heart hemodynamics (particularly PVR) in CTEPH. Because PVR is difficult to estimate noninvasively—and yet correlates with disease severity—the RV Tei index may be a valuable noninvasive parameter for monitoring disease severity in CTEPH and outcome after PTE.