Incremental doses of intracoronary adenosine for the assessment of coronary velocity reserve for clinical decision making.

Achievement of maximal vasodilatation of the coronary microcirculation is a prerequisite for the measurement of coronary flow reserve (CFR). The present study was designed to address the hypothesis that intracoronary adenosine yields more complete vasodilation of the coronary microcirculation when incremental doses are used, resulting in higher and more accurate coronary flow reserve measurements. Four hundred and fifty-seven patients were divided in two groups; group I (319 patients) comprised patients without angiographic evidence of significant coronary artery disease, while group II (138 patients) comprised patients with intermediate coronary stenoses (between 40% and 70% diameter stenosis). Coronary velocity reserve (CVR, a surrogate measurement for CFR) was measured during cardiac catheterization using a Doppler-tipped guidewire. Incremental doses of intracoronary adenosine (12 to 54 microg for the left coronary artery and 6 to 42 microg for the right coronary artery) were administered. There was a significant difference between the initial dose of adenosine and the subsequent incremental doses. Of a total of 479 observations, only 192 (40%) had the maximal CVR value at the first dose. Thirty-nine percent of the patients in group I and 27% in group II with an initial CVR value < 2.5 increased CVR to > or = 2.5 with incremental doses of adenosine. This study suggests that incremental doses of adenosine should be used to achieve maximal CVR for the assessment of the functional significance of coronary lesions. Cathet Cardiovasc Intervent 2001;54:34-40.

Noninvasive assessment of left ventricular end-diastolic pressure by the response of the transmitral a-wave velocity to a standardized Valsalva maneuver.

Impaired relaxation is frequently masked by elevated filling pressures, resulting in a pseudonormal flow pattern (E/A >1.0). Because the E/A wave ratio increases as filling pressures rise, it is generally assumed that patients with an E/A ratio of <1.0 (impaired relaxation pattern) have relatively low filling pressures. Nevertheless, patients with an E/A ratio of <1.0 can have as profoundly elevated filling pressures as patients with a pseudonormal or restrictive filling pattern. Because left ventricular (LV) pressure during end-diastole essentially determines atrial afterload, the response of the A-wave velocity to a reduction of atrial afterload by a standardized Valsalva maneuver should allow estimation of LV end-diastolic pressure (LVEDP) regardless of the baseline Doppler flow pattern. This was tested in 20 consecutive patients who were studied by pulse-wave Doppler echocardiography during cardiac catheterization. There was a close correlation between LVEDP and the change in A-wave velocity during the Valsalva maneuver (r = 0.85, SEE 6.7 mm Hg) regardless of the baseline E/A ratio. In patients with a LVEDP of <15 mm Hg the A wave decreased by 21 +/- 15 cm/s. In patients with a LVEDP of >25 mm Hg the A wave increased by 18 +/- 13 cm/s. The change in the E/A ratio during Valsalva correlated fairly with LVEDP (r = -0.72, SEE 8.8 mm Hg), the baseline E/A ratio correlated poorly, and scatter was substantial (r = 0.46, SEE 11.2 mm Hg). Just as elevated filling pressures can mask impaired relaxation, the impaired relaxation pattern can mask the presence of elevated filling pressures. This can be revealed by testing the response of the A wave to the Valsalva maneuver, allowing estimation of LVEDP independent of the baseline E/A ratio.

Assessment of pseudohypertrophy as a measure of left-ventricular compression in patients with cardiac tamponade.

BACKGROUND: Left-ventricular pseudohypertrophy reflecting left-ventricular compression was reported in a selected group of patients with cardiac tamponade. HYPOTHESIS: Criteria for the presence of pseudohypertrophy can be established to guide its use as a sign of left-ventricular compression in patients with cardiac tamponade. METHODS: Left-ventricular wall thickness, diameters, relative diastolic wall thickness (%) = (posterior wall thickness/end diastolic radius) x 100 and estimated left-ventricular mass were measured in patients with small, moderate and large pericardial effusion, in patients with cardiac tamponade before and after pericardiocentesis (16 patients in each group) and in 30 control subjects with normal echocardiograms. RESULTS: Left-ventricular posterior wall thickness was increased (12 +/- 2 vs. 9 +/- 1 mm, p < 0.001), left-ventricular end-diastolic diameter was reduced (3.9 +/- 0.5 vs. 4.6 +/- 0.3 cm, p < 0.001) and relative left-ventricular diastolic wall thickness was increased (61 +/- 13 vs. 41 +/- 4.5%, p < 0.001) only in patients with cardiac tamponade compared to controls, but not in patients with small, moderate and large effusions, respectively (relative wall thickness: 42 +/- 5, 41 +/- 7 and 44 +/- 7%, p = NS). Mean values of the estimated left-ventricular mass were similar in all groups. Following pericardiocentesis all parameters were normal. CONCLUSIONS: Despite normal left-ventricular mass, relative left-ventricular diastolic wall thickness is elevated in patients with cardiac tamponade. In contrast it is normal in patients with various degrees of pericardial effusion supporting its use as a quantitative measure of left-ventricular compression in patients with suspected cardiac tamponade.

The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA.

OBJECTIVES: To determine the prevalence and clinical significance of early ST segment elevation resolution after primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI). BACKGROUND: Despite angiographically successful restoration of coronary flow early during AMI, adequate myocardial reperfusion might not occur in a substantial portion of the jeopardized myocardium due to microvascular damage. This phenomenon comprises the potentially beneficial effect of early recanalization of the infarct related artery (IRA). METHODS: Included in the study were 117 consecutive patients who underwent angiographically successful [Thrombolysis in Myocardial Infarction (TIMI III)] primary PTCA. The patients were classified based on the presence or absence of reduction > or =50% in ST segment elevation in an ECG performed immediately upon return to the intensive cardiac care unit after the PTCA in comparison with ECG before the intervention. RESULTS: Eighty-nine patients (76%) had early ST segment elevation resolution (Group A) and 28 patients (24%) did not (Group B). Group A and B had similar clinical and hemodynamic features before referring to primary PTCA, as well as similar angiographic results. Despite this, ST segment elevation resolution was associated with better predischarge left ventricular ejection fraction (LVEF) (44.7 +/- 8.0 vs. 38.2 +/- 8.5, p < 0.01). Group B patients, as compared with those of Group A, had a higher incidence of in-hospital mortality (11% vs. 2%, p = 0.088), congestive heart failure (CHF) [28% vs. 19%, odds ratio (OR) = 4, 95% confidence interval (CI) 1 to 15, p = 0.04], higher long-term mortality (OR = 7.3, 95% CI 1.9 to 28, p = 0.004 with Cox proportional hazard regression analysis) and long-term CHF rate (OR = 6.5, 95% CI 1.3 to 33, p = 0.016 with logistic regression). CONCLUSIONS: Absence of early ST segment elevation resolution after angiographically successful primary PTCA identifies patients who are less likely to benefit from the early restoration of flow in the IRA, probably because of microvascular damage and subsequently less myocardial salvage.

Transient bradycardia induced by carotid sinus pressure increases outflow obstruction in hypertrophic obstructive cardiomyopathy but not in valvular aortic stenosis.

BACKGROUND: The murmur of hypertrophic obstructive cardiomyopathy (HOCM) increases in intensity in about 80% of those patients in whom carotid sinus pressure (CSP) slows the heart rate. This does not occur in valvular aortic stenosis (AS). STUDY OBJECTIVES, DESIGN, AND PATIENTS: It was hypothesized that left ventricular (LV) obstruction increases with CSP in HOCM and not in AS. Furthermore, it was not clear whether it was the sudden bradycardia or CSP itself that was responsible for the effect noted. Therefore, studies were performed using two different interventions: (1) Doppler echocardiography was performed before and during CSP in 36 HOCM patients and 21 AS patients; (2) two patients with DDD pacemakers and HOCM were examined before and after pacemaker rate slowing. Finally, atrial pacing was performed in three HOCM patients at catheterization, and atrial pacing was either slowed or stopped (without CSP). RESULTS: LV outflow velocity and pressure gradient increased in 28 of 30 HOCM patients (92%) in whom heart rate decreased with CSP. The peak instantaneous pressure gradient increased from 45+/-37 to 77+/-53 mm Hg (p<0.005), and the velocity contour became more typical of HOCM. The pressure gradient increased from 30 mm Hg to 64 and 81 mm Hg, respectively, in the two patients with DDD pacemakers after pacemaker rate slowing. Similar results were seen with slowing or cessation of atrial pacing at catheterization. In contrast, the pressure gradient increased in only three of 21 AS patients (14%), to 44+/-28 from 41+/-25 mm Hg, and remained unchanged in the other 18. CONCLUSION: This study shows that LV outflow velocity and pressure gradient increase markedly in most HOCM patients (92%) if CSP succeeds in slowing the heart rate, but not in patients with valvular AS. A similar effect is obtained by simply decreasing the atrial rate in patients with DDD or atrial pacemakers. This increase in outflow tract obstruction is sufficient to account for the increase in murmur intensity. Decreased afterload (secondary to greater aortic decompression with the longer diastole), increased intrinsic force of contraction with the bradycardia (the Woodworth effect), and Starling's law may play independent roles in the dynamic increase in obstruction observed during CSP in patients with HOCM. Worsening of mitral regurgitation was not clearly shown to contribute to the increase in murmur, but it cannot readily be ruled out.

Rescue coronary angiography after failed thrombolysis: a real-life experience.

Failed thrombolysis in acute myocardial infarction (AMI) patients is associated with a high risk of morbidity and mortality. Rescue or salvage percutaneous transluminal coronary angioplasty (PTCA) in this group of patients is still controversial. We report our experience with early emergency angiography and rescue PTCA in 27 patients who were hemodynamically unstable or had a large area of myocardium at risk after failed thrombolysis. Rescue PTCA was successful in 95% of attempted PTCA. Three patients were referred to emergency CABG. Early 'rescue angiography' with or without rescue PTCA after failed thrombolysis in a selected patient population, is an important tool for early risk stratification and decision-making during the hyperacute phase of AMI, while it may also serve in restoring coronary artery patency of the infarct-related artery with a high success rate.

Coronary arterioluminal communications in routine angiography.

Visualization of the left ventricular cavity from coronary arterioventricular communications is rarely encountered in routine coronary angiography. We report 14 patients, of 5,500 consecutive cardiac catheterizations, in whom these communications were evident during coronary angiography. All 14 patients had angina pectoris; in each the arterioluminal communication originated from the left anterior descending coronary artery. Two patients had evidence of anterior wall ischemia despite a normal left anterior descending coronary artery, suggesting that a possible steal phenomenon is responsible for the myocardial ischemia.

Echocardiographic left ventricular remodeling and pseudohypertrophy as markers of hypovolemia. An experimental study on bleeding and volume repletion.

BACKGROUND: Monitoring intravascular volume during surgery, especially in major cardiovascular procedures is necessary for appropriate fluid restoration and the maintenance of an adequate cardiac output. In estimating preload, both standard hemodynamic and echocardiographic parameters have been limited. The purpose of this study was to further define the effects of induced hypovolemia on the echocardiographic parameters. In particular, we sought to show whether a decrease in echocardiographic left ventricular area and volume was associated with a significant increase in left ventricular wall thickness (left ventricular pseudohypertrophy) and with changes in LV function. In addition, we sought to investigate the effects of rapid restoration of blood volume on cardiac dimensions and function. METHODS AND RESULTS: Seven anesthetized pigs underwent systemic and right heart pressures and cardiac output measurements. Two-dimensional echocardiographic parasternal long- and short-axis views were obtained during graded bleeding by rapid withdrawal of blood from an arterial cannula, with increments of 5% each up to 30% of calculated blood volume. After completion of the bleeding, the entire amount of the blood withdrawn was retransfused within 4 to 5 minutes. Both hemodynamic and echocardiographic measurements were performed at baseline, immediately after the completion of each stage of bleeding and after blood restoration. Mean (+/- standard deviation) left ventricular wall thickness (mean of septal and posterior wall thickness) was 6.3 +/- 0.1 mm at baseline, 8.3 +/- 1.5 mm at peak bleeding, and 6.2 +/- 0.1 after restoration (p < 0.01). Left ventricular mass did not change during the experiment. Left ventricular end-diastolic volume was 62.8 +/- 20.3 ml at baseline, 37.5 +/- 12.4 ml at peak bleeding (p < 0.0001), and 65.9 +/- 16.7 ml after blood restoration (p < 0.001 compared with 30% bleeding). H/r ratio (posterior wall thickness divided by left ventricular radius) increased from 0.29 +/- 0.07 at baseline to 0.50 +/- 0.19 at peak bleeding returning to 0.26 +/- 0.04 after restoration. Left ventricular ejection fraction was 0.53 +/- 0.10 at baseline and 0.55 +/- 0.20 at peak bleeding (not significant), decreasing to 0.38 +/- 0.11 after blood restoration (p < 0.05 compared with 30% bleeding). End-diastolic volume correlated closely with right atrial pressure (r = -0.82), capillary wedge pressure (r = -0.78), and stroke volume (r = 0.74). Left ventricular ejection fraction inversely correlated with left ventricular end-diastolic volume (r = -0.48) and with end-systolic wall stress (r = -0.62). The changes in interventricular septal and posterior wall thickness were inversely related to left ventricular end-diastolic volume (r = -0.72 and -0.35, respectively). CONCLUSIONS: This study shows that transient concentric left ventricular remodeling (pseudohypertrophy), a phenomenon previously described in cardiac tamponade and during rapid atrial pacing is commonly seen during hypovolemia. This new sign may further enhance the echocardiographic estimation of left ventricular preload.

Exogenous insulin-like growth factor II enhances post-infarction regional myocardial function in swine.

OBJECTIVES: Insulin-like growth factor II (IGF-II) promotes cardiac myocyte growth and contractility in vitro. This study was designed to investigate the effect of exogenous IGF-II on regional myocardial function at the area of infarct in the pig. METHODS: Myocardial infarction was induced in 12 female anaesthetized pigs by affigel blue beads, embolizing microvessels of the left anterior descending coronary artery distribution. In the experimental group (n = 6), IGF-II (0.12 microgram.kg-1 in two animals and 0.6 microgram.kg-1 in four) was incorporated into the beads and delivered by them to the infarct area. Myocardial function was followed echocardiographically, and the excised heart was analysed immunohistochemically and histopathologically. RESULTS: Myocardial function in injured zones, inversely related to an echocardiographic segmental wall motion score (mean +/- SEM), was similar between the two groups at baseline, but at 4 weeks post-infarction was significantly (P = 0.008) reduced in the control group (0.58 +/- 0.38 vs 3.42 +/- 0.84), in contrast to nearly baseline values in the experimental group (0.58 +/- 0.33 vs 1.17 +/- 0.42, P = 0.41). Cardiac performance in injured segments was significantly better after myocardial injury in the experimental group (P = 0.04). Tissue samples from both groups (4 weeks post-infarction), stained with haematoxylin and eosin demonstrated peri-infarct myocyte hypertrophy, corresponding to regions selectively stained by an antibody for CD56, which highlights growing cardiac myocytes. By image analysis semi-quantification, staining for CD56 was significantly (P = 0.04) higher in the peri-infarct region of the experimental group, as compared with controls (106.5 +/- 2.8 vs 92 +/- 4.4 gray level units). Microvessels stained for von-Willebrand factor were similar in number in both groups (P = 0.8), as were mesenchymal cells stained for vimentin (P = 0.7). CONCLUSIONS: Exogenous IGF-II, delivered to the infarct area ameliorates regional cardiac function in the pig, perhaps by inducing peri-infarct myocyte growth.

Percutaneous balloon pericardiostomy for treatment of cardiac tamponade.

Percutaneous balloon pericardiostomy was performed in eight severely ill patients with malignancy (seven patients) and chronic renal failure (one patient). To investigate the feasibility of balloon pericardiostomy as a bedside procedure, echocardiography was used in addition to fluoroscopy in monitoring the procedure. The pericardium was entered from the standard subxiphoid site. An 18 to 25 mm, 3 or 4 cm long, balloon catheter, introduced over a stiff guidewire was inflated across the parietal pericardium. Creation of a pericardial opening was obtained in each of the eight patients. Bleeding from the needle entry site was the only complication observed in one patient. The balloon catheter could be localized by echocardiography only in 2/8 cases. Two patients died, 3 and 14 days after the procedure, from the primary disease; six patients were still alive at follow-up ranging from 32 to 342 days. No recurrence of cardiac tamponade was observed in any patient. Percutaneous balloon pericardiostomy is efficacious and safe in relieving pericardial tamponade and preventing its recurrence in severely ill patients. Fluoroscopy is needed to monitor the procedure. The value of echocardiography is limited for follow-up controls of pericardial effusion.

Acquired left ventricular-right atrial communication caused by infective endocarditis detected by transesophageal echocardiography: case report and review of the literature.

Acquired left ventricular-right atrial communication due to infective endocarditis was diagnosed in a 64-year-old patient by transesophageal echocardiography and confirmed by cardiac catheterization. The patient was initially treated medically and then referred for corrective surgery.

Decreased thickening of normal myocardium with transient increased wall thickness during stress echocardiography with atrial pacing.

Stress echocardiography is used increasingly in the evaluation of coronary artery disease. The echocardiographic evaluation of ischemia is based on stress-induced changes in wall motion and wall thickening of the ischemic segments. Studies have demonstrated that left ventricular volumetric changes may induce changes in wall thickness. The aim of the study was to evaluate whether significant changes in ventricular volume, wall thickness, and wall thickening occur during stress echocardiography with atrial pacing. Seven German Landrace female pigs were studied 4 weeks after the induction of a small myocardial infarction. Echocardiographic measurements were conducted in noninfarcted segments on the short-axis view at baseline and during atrial pacing at 120, 150, and 180 beats/min. End-diastolic circumferential area decreased from 12.3 +/- 2.0 cm2 at baseline to 8.9 +/- 1.9 cm2 at 180 beats/min of atrial pacing (p < 0.01). Mean wall thickness (interventricular septal plus posterior wall thickness divided by 2) increased markedly and progressively from 6.7 +/- 0.6 mm at baseline to 9.8 +/- 1.0 mm at 180 beats/min (p < 0.01). The increase in wall thickness correlated inversely with end-diastolic area (r = -0.57; p < 0.01). Percent systolic thickening decreased from 38.9 +/- 12.0 at baseline to 14.9 +/- 7.4 at 180 beats/min of atrial pacing (p < 0.01). The decrease in percent wall thickening correlated with the increase in wall thickness (r = -0.71; p < 0.01). In conclusion, this study shows that a marked increase in wall thickness (pseudohypertrophy) and decrease in percent systolic thickening are observed during rapid atrial pacing in normal myocardium and do not indicate stress-induced left ventricular dysfunction.

Intracoronary injection of basic fibroblast growth factor enhances angiogenesis in infarcted swine myocardium.

OBJECTIVES: This study was performed to examine the effect of intracoronary exogenous basic fibroblast growth factor (bFGF) on angiogenesis in infarcted myocardial regions. BACKGROUND: Exogenous bFGF is a potent promoter of angiogenesis. Little information is available on its effect on myocardial angiogenesis. METHODS: Myocardial infarction was induced in 10 pigs by intracoronary injection of microscopic beads. Four pigs served as a control group; in six pigs slow-release bFGF was delivered by the beads. Cardiac performance was evaluated by repeated echocardiographic measurement and angiogenesis was evaluated by immunohistochemical studies 14 days later. RESULTS: As compared with control pigs, pigs treated with bFGF had higher microvessel counts (mean +/- SEM) in both viable tissue (141 +/- 27 per field vs. 39 +/- 4, p = 0.01) and nonviable tissue (329 +/- 26 per field vs. 95 +/- 7, p < 0.001) within the infarct area. No significant differences in total regional left ventricular wall motion were noted between the two groups throughout the 14-day study period. CONCLUSIONS: In the swine, direct intracoronary application of bFGF to infarcted myocardium enhances myocardial neovascularization within 2 weeks.

Balloon aortic valvuloplasty in the elderly: useful when there is no alternative.

Of 63 elderly patients with calcific aortic stenosis in whom balloon aortic valvuloplasty was performed, 26 treated with the new technique of Cribier and Letac are the subject of this report. Patients were referred for the procedure because they were at high surgical risk, or were not candidates for surgery. Seven matched patients who fit the criteria for balloon valvuloplasty but refused the valvuloplasty procedure served as controls. Aortic gradient decreased from 78 +/- 27 mm Hg to 35 +/- 20 mm Hg and aortic valve area increased from 0.47 +/- 0.16 cm2 to 0.83 +/- 0.38 cm2 (P < 0.0001). Symptomatic improvement was immediately obtained in each patient. Complications were rare, with only one patient needing vascular repair for femoral artery occlusion. Three patients died during the initial hospitalization (none during the procedure). Valvuloplasty patients were followed for a mean period of 9.6 +/- 9.4 months. Three months survival was 87%, 6 months survival was 76%, and 12 months survival was 61%. Four of seven patients in the control group (57%) died within 3 months after initial referral. Balloon aortic valvuloplasty is a useful treatment in elderly patients who are poor surgical candidates. It may have a positive influence on short-term survival.

Left ventricular pseudohypertrophy in cardiac tamponade: an echocardiographic study in a canine model.

OBJECTIVES: This study was designed to establish whether left ventricular pseudohypertrophy in cardiac tamponade can be reproducibly induced in an experimental canine model and to investigate the mechanism of its production. BACKGROUND: Past experimental and clinical studies have shown reduction of ventricular volumes resulting from cardiac tamponade. Left ventricular pseudohypertrophy, a transient thickening of myocardial walls, was recently described as a new echocardiographic sign of cardiac tamponade. METHODS: Cardiac tamponade was induced in seven anesthetized open chest dogs with serial bolus injections of 50 ml each of 0.9% saline solution into the pericardial sac. Under hemodynamic monitoring, M-mode and two-dimensional echocardiographic measurements were performed from a right parasternal window at each stage of graded cardiac tamponade. RESULTS: There was a progressive increase of interventricular septal and posterior wall diastolic thickness. Mean wall thickness (interventricular septal thickness + posterior wall thickness divided by 2) was 9.8 +/- 1.3 mm at baseline, 14.3 +/- 0.9 mm at peak tamponade and 9.0 +/- 1.5 mm after fluid withdrawal (p < 0.0001). Mean wall thickness correlated directly with the severity of cardiac tamponade, as estimated from the level of right arterial pressures (r = 0.75 and p < 0.0001), and with the decrease of left ventricular cavity volume (r = -0.67 and p < 0.0001). Left ventricular mass did not change significantly. CONCLUSIONS: Left ventricular pseudohypertrophy is a constant manifestation of cardiac tamponade in a canine model. The degree of myocardial thickening correlates with the reduction of ventricular dimensions and with the severity of hemodynamic compromise, representing a constant facet of heart remodeling in cardiac tamponade.

The effect of venous occlusion with tourniquets on peripheral blood pooling and ventricular function.

Rotating tourniquets were once part of the traditional treatment of acute pulmonary edema. Their effectiveness has been questioned and vasodilator therapy has replaced them, but early favorable results suggested that they may play a beneficial role. A radioisotope technique was used to evaluate blood volume increments in the leg after venous occlusion at 60 mm Hg in 26 patients with left ventricular dysfunction following myocardial infarction. Mean radionuclide counts (reflecting the blood volume distal to the occlusion) increased from the preocclusion value. Thus, satisfactory trapping of blood is achieved. However, mean left ventricular ejection fraction (EF) decreased slightly but significantly and this decrease in EF was observed in 18 of 26 patients. Left ventricular end-diastolic and end-systolic volume equivalents tended to decrease slightly but not in all patients. Mean stroke volume and cardiac output equivalents were reduced by 14 percent while peripheral resistance increased significantly. The present study thus fails to support the hypothesis that preload reduction by tourniquets improves left ventricular function; the exact opposite effect may occur because of increased afterload.

Color Doppler echocardiography of isolated cleft mitral valve. Roles of the cleft and the accessory chordae.

To study the mechanism of altered mitral function in the presence of an isolated cleft mitral valve (ICMV) with regard to the relative roles of the cleft and of the accessory chordae, seven patients with ICMV were studied with color Doppler echocardiography. Mitral insufficiency ranging from mild to severe was demonstrated in six cases. The regurgitant jet originated in each case from the site of the cleft: in five patients the regurgitant jet had a narrow base originating exactly from the cleft; in the sixth patient, the regurgitant flow presented as a broad-based jet suggesting that accessory chordae restricted the motion of the anterior mitral leaflet. Turbulent flow in the left ventricular outflow tract, starting at the level of the accessory chordae, was found in one patient in whom a pressure drop of 44 mm Hg was detected with continuous-wave Doppler imaging. The altered function of the mitral valve cleft stems from two elements, the cleft itself and the accessory chordae. Color Doppler flow imaging showed that the cleft was the main factor causing mitral insufficiency. The accessory chordae played an additional pathogenetic role in two patients by causing restricted mitral motion or left ventricular outflow tract obstruction.

Intrapericardial extralobar pulmonary sequestration in a neonate.

A huge pericardial effusion was diagnosed during fetal ultrasound examination performed in the 42nd week of pregnancy on a healthy 25-year-old woman. Immediately after the birth, a two-dimensional echocardiogram confirmed this finding in the infant, and an intrapericardial kidney-shaped solid mass measuring 45 x 56 x 15 mm, completely surrounded by pericardial effusion, was visualized to the left part of the heart. The heart was normal. No signs of cardiac tamponade were seen. At the age of two days, the mass was surgically resected and the pericardial fluid evacuated. Microscopic examination revealed that the mass was formed totally of normal lung tissue surrounded by normal pleura. To the best of our knowledge, this is the first case of intrapericardial extralobar sequestration consisting of an accessory lung with completely normal lung tissue.