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We report a case of localised pericardial constriction leading to right ventricular outflow tract obstruction. Localised pericardial constriction is rare, but the diagnosis should be considered in patients who present with recurrent pericardial constriction following previous partial pericardiectomy. Close attention to physical findings may enable the diagnosis to be made prior to cardiac catheterisation.
Doppler ultrasound recordings of velocities of flow across the mitral and tricuspid valves and in the hepatic veins, and their variation with respiration, were recorded in seven patients with constrictive pericarditis and in six patients with restrictive cardiomyopathy. Deceleration of mitral and tricuspid flow was also evaluated during apnea. Color flow Doppler was performed in order to evaluate mitral and tricuspid regurgitation. Eight healthy adults served as controls. The patients with constrictive pericarditis showed higher peak diastolic velocities of mitral flow, as well as marked increase of velocity of flow at the onset of expiration and decrease at the onset of inspiration. Reciprocal respiratory variation of the velocities were also observed across the tricuspid valve. The patients with restrictive cardiomyopathy showed moderate or severe mitral and tricuspid regurgitation. They also showed shorter deceleration of flow across the mitral and tricuspid valves during apnea. The pattern of flow in the hepatic veins showed reversal during systole with accentuated reversion during inspiration. These results suggest that patient with constrictive pericarditis and restrictive cardiomyopathy can be differentiated by comparing Doppler echocardiographic data, along with changes induced by respiration.
To clarify the role of serotonin in eliciting myocardial ischemia, the effects of serotonin on coronary vasculature and cardiac performance were examined in anesthetized open chest dogs. Without coronary stenosis, intracoronary infusion of serotonin (0.001 to 1.0 micrograms/kg per min) for 40 s caused dose-dependent increases in coronary blood flow up to 175 +/- 8.3%. During fixed coronary stenosis produced by a metal constrictor that restricted active vasomotion of the stenosed segment, only the highest dose of serotonin increased coronary blood flow by 23 +/- 5.7% and decreased distal coronary pressure without any changes in stenosis resistance and systemic hemodynamic variables. During dynamic coronary stenosis created by inflation of an intraluminal microballoon that preserved active vasomotion of the stenosed segment, intracoronary serotonin (0.1 and 1.0 micrograms/kg per min) evoked marked decreases in coronary blood flow and distal coronary pressure and an increase in stenosis resistance, resulting in an elevation of left ventricular end-diastolic pressure and worsening of left ventricular dP/dt. These deleterious effects were reversed by additive intracoronary infusion of nitroglycerin (10 micrograms/min). The detrimental effects of serotonin were not attenuated by pretreatment with aspirin (10 mg/kg, intravenously), which suppressed adenosine disphosphate- and arachidonic acid-induced platelet aggregation in vitro. Furthermore, intracoronary infusion of serotonin (0.1 and 1.0 micrograms/kg per min) from the site distal to coronary stenosis failed to decrease coronary blood flow during dynamic coronary stenosis. Therefore, these detrimental effects of serotonin during dynamic coronary stenosis could be caused by constriction of a large coronary artery but not by platelet aggregation. Vascular effects of serotonin without coronary stenosis and with dynamic coronary stenosis were inhibited by pretreatment with methysergide (0.3 mg/kg, intravenously), but not with ketanserin (0.5 mg/kg, intravenously) which inhibited serotonin-induced platelet aggregation in vitro. Thus, serotonin produced opposing effects on coronary vasculature, that is, small coronary artery dilation and large coronary artery constriction. Both vascular effects were mediated by non-S2-serotonergic receptor activation of the coronary artery. The data obtained in this study suggest that serotonin-elicited constriction of a large coronary artery may play a crucial role in the pathogenesis of myocardial ischemia during pliable coronary stenosis.
The purposes of this study are to determine the stability of surgical mandibular constriction with a midline osteotomy and to evaluate the periodontal and temporomandibular joint responses. A symphyseal osteotomy to facilitate mandibular construction was performed in 15 patients to correct transverse discrepancies. At the same time a surgical anterior or posterior repositioning of the mandible was done by using a bilateral sagittal osteotomy of the vertical ramus. Tomograms in the coronal plane including the mandibular second molars were taken preoperatively (T1), immediately postoperatively (T2) and 8 weeks postoperatively (T3). Linear measurements between the cortical borders of the mandible were assessed from the tomograms at each time period. Median surgical and postoperative changes in mandibular width were determined. When evaluating the entire group no statistically significant change in the surgical constriction was found postoperatively (T2 and T3), although there was some individual variability. An examination of the periodontal response at the osteotomy site revealed no statistically significant change between the initial and the 5-month postoperative examinations. No changes in joint noise were detected postoperatively, and all mandibular joint movements returned to preoperative values except for excursive movements. Mandibular constriction with a midline osteotomy on conjunction with a bilateral sagittal osteotomy was found to be a stable modality for correcting transverse disharmonies.
The pericardium envelopes the cardiac chambers and under physiological conditions exerts subtle functions, including mechanical effects that enhance normal ventricular interactions that contribute to balancing left and right cardiac outputs. Because the pericardium is non-compliant, conditions that cause intrapericardial crowding elevate intrapericardial pressure, which may be the mediator of adverse cardiac compressive effects. Elevated intrapericardial pressure may result from primary disease of the pericardium itself (tamponade or constriction) or from abrupt chamber dilatation (eg, right ventricular infarction). Regardless of the mechanism leading to increased intrapericardial pressure, the resultant pericardial constraint exerts adverse effects on cardiac filling and output. Constriction and restrictive cardiomyopathy share common pathophysiological and clinical features; their differentiation can be quite challenging. This review will consider the physiology of the normal pericardium and its dynamic interactions with the heart and review in detail the pathophysiology and clinical manifestations of cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy.
BACKGROUND: In most primary myocardial diseases, early diastolic mitral annulus velocity (E') decreases with disease progression. To our knowledge, constrictive pericarditis (CP) is the only condition without this phenomenon. OBJECTIVE: This study was performed to evaluate the diagnostic and pathophysiologic role of mitral annulus velocity in patients with CP. METHODS: In all, 17 patients with CP (9 men; mean age 46.5 +/- 14.3 years), 8 patients with cardiac tamponade (Tamp) (2 men; mean age 44.5 +/- 15.0 years), and age- and sex-matched control subjects for CP and Tamp were recruited for the study. Early mitral inflow velocity and E' were obtained while simultaneously recording respiration. In 8 patients with CP and in all patients with Tamp, these measurements were repeated after the relief of constrictive physiology or after pericardiocentesis. RESULTS: In patients with CP, E' was significantly higher than it was for control subjects (12.9 +/- 3.0 cm/s vs 9.8 +/- 2.4 cm/s, P <.01). An E' of 2 cm/s higher than the predicted normal E' could differentiate patients with CP from control subjects with a sensitivity of 76% and specificity of 82%. In 12 of 17 patients (71%), inspiratory E' was higher than expiratory E'-the opposite of mitral inflow variation. In 8 patients, E' decreased significantly after the relief of constrictive physiology (13.8 +/- 2.5 cm/s vs 9.3 +/- 3.1 cm/s, P <.05). In contrast, E' in the Tamp group was significantly lower than in the control group (6.8 +/- 1.6 cm/s vs 10.2 +/- 2.5 cm/s, P <.01), did not show significant respiratory variation, and increased significantly after pericardiocentesis (6.8 +/- 1.6 cm/s vs 9.5 +/- 3.0 cm/s, P <.05). CONCLUSION: E' is exaggerated in CP, which is helpful for diagnosis. The opposite phenomenon was noted in Tamp, a dissimilarity that might contribute to different hemodynamics.
This study was conducted to examine the role of nitric oxide (NO) in peripheral neuropathy induced by chronic constriction injury of sciatic nerve of rats by using NO precursor, NO donors and nitric oxide synthase (NOS) inhibitors. Chronic constriction injury of sciatic nerve of rats resulted in peripheral neuropathy as confirmed by nociceptive behavioural tests using mechanical, thermal and cold allodynia. NO precursor, L-arginine and NO donors sodium nitroprusside, S-nitroso-N-acetylpenicillamine potentiated the hyperalgesia and allodynia significantly suggesting proalgesic effect in neuropathic rats. Intracerebroventricular (i.c.v.) administration of rats with NOS inhibitors such as L-N(G)-nitroarginine methyl ester, N-iminoethyl lysine and 7-nitroindazole did not show any effect but i.p. administration of NOS inhibitors aminoguanidine, L-N(G)-nitroarginine methyl ester and 7-nitroindazole caused alleviation of pain. The study confirms the involvement of endogenously synthesized and exogenously administered NO in chronic constriction injury-induced neuropathy in rats. Significant increase in the levels of nitrate and nitrite in ligated sciatic nerve suggest that local up regulation of NO in the production and maintenance of neuropathic pain. In conclusion, initial attempt to manipulate L-arginine: NO pathway is indicative of therapeutic potential of these interventions in the management of neuropathic pain.
Constrictive pericarditis is a rare heart disease but potentially curable with pericardiectomy. Conventional image modalities such as echocardiography, CT and MRI have been used as useful diagnostics for constrictive pericarditis. However, they have limitations in delineating accurate extent of calcified pericardium three-dimensionally (3-D) to aid the surgical management to release the constricted chambers. We present a patient with typical severe extensive myopericardial calcifications visualized by 3-D multidetector CT who was successfully treated by pericardiectomy.
OBJECTIVES: We sought to determine the association of etiology of constrictive pericarditis (CP), pericardial calcification (CA), and other clinical variables with long-term survival after pericardiectomy. BACKGROUND: Constrictive pericarditis is the result of a spectrum of primary cardiac and noncardiac conditions. Few data exist on the cause-specific survival after pericardiectomy. The impact of CA on survival is unclear. METHODS: A total of 163 patients who underwent pericardiectomy for CP over a 24-year period at a single surgical center were studied. Constrictive pericarditis was confirmed by the surgical report. Vital status was obtained from the Social Security Death Index. RESULTS: Etiology of CP was idiopathic in 75 patients (46%), prior cardiac surgery in 60 patients (37%), radiation treatment in 15 patients (9%), and miscellaneous in 13 patients (8%). Median follow-up among survivors was 6.9 years (range 0.8 to 24.5 years), during which time there were 61 deaths. Perioperative mortality was 6%. Idiopathic CP had the best prognosis (7-year Kaplan-Meier survival: 88%, 95% confidence interval [CI] 76% to 94%) followed by postsurgical (66%, 95% CI 52% to 78%) and postradiation CP (27%, 95% CI 9% to 58%). In bootstrap-validated proportional hazards analyses, predictors of poor overall survival were prior radiation, worse renal function, higher pulmonary artery systolic pressure (PAP), abnormal left ventricular (LV) systolic function, lower serum sodium level, and older age. Pericardial calcification had no impact on survival. CONCLUSIONS: Long-term survival after pericardiectomy for CP is related to underlying etiology, LV systolic function, renal function, serum sodium, and PAP. The relatively good survival with idiopathic CP emphasizes the safety of pericardiectomy in this subgroup.
OBJECTIVE: The risk of failure of root canal therapy was assessed in teeth with inaccessible apical constriction and factors influencing treatment outcome in these teeth were analyzed. METHODS: From the same 57 patients, one tooth with inaccessible apical constriction (n=57) and one tooth with adequate accessibility (n=57) were included in this retrospective investigation. Cox regression analysis was used to analyze factors that may have influenced the outcome one or more years after obturation. These factors included inaccessibility, systemic disease, canal curvature, preoperative periradicular lesion, widening of periodontal ligament space, patient gender and age, size of master apical file, preoperative pulp vitality, years of operator experience and obturation length. RESULTS: Inaccessible apical constriction was a significant factor related to outcome (odds ratio, 5.301). Preoperative presence of periradicular lesion significantly influenced the outcome in cases with inaccessibility (odds ratio, 4.448). CONCLUSION: Inaccessibility increases the risk of root canal therapy failure particularly in teeth with preoperative periradicular lesion.
Among the various etiologies of compressive lesions, the development of an hourglass-like constriction of the nerve that is unrelated to any recognizably compressive structure is a very rare phenomenon. This problem has been reported previously for the radial nerve and its branch posterior interosseous nerve and for the anterior interosseous nerve, a branch of median nerve. Here we report 2 cases of hourglass-like constriction of the axillary nerve that were observed during surgery; the constrictive segment was unrelated to any compressive structure.
The purpose of this study was to evaluate the glottis constriction response induced by a sudden and involuntary increase in gastric and oesophageal pressures by Tll-Ll intervertebral magnetic stimulation of the abdominal muscle roots in nine healthy subjects. Twitch flow, twitch gastric, and oesophageal pressures were measured after abdominal muscle root stimulation, which allowed pharyngo-laryngeal muscle activation to be characterized. Pharyngeal endoscopies were performed on five subjects to assess vocal cord movements. All stimulations induced positive gastric and oesophageal pressures and expiratory flow, which increased with stimulation intensity (flow: R=0.32; p<0.0001; oesophageal pressure: R=0.26; p=0.001; gastric pressure: R=0.37; p<0.0001). Twitch gastric pressure and twitch oesophageal pressure were negatively correlated with twitch flow (respectively, R=-0.183, p<0.05; R=-0.35, p<0.0001). Upper airway resistance was higher at peak oesophageal pressure than at peak flow (p<0.001). Peak twitch gastric and twitch oesophageal pressure latencies were similar (133+/-4ms and 122+/-4ms) but longer than peak twitch flow and EMG latencies (62+/-2ms and 73+/-4ms, p<0.0001). Glottis constriction following magnetic abdominal muscle root stimulation was seen in all subjects during endoscopy, with a latency estimated at between 80 and 100ms. This method could be a new, simple tool for assessing the upper airway constriction protective reflex.
The purpose of this study was to examine the usefulness of pulsed tissue Doppler imaging for diagnosing constrictive pericarditis. Motion velocities of the ventricular septum (VS) and left ventricular (LV) posterior wall along the short axis, and those of the anterior right ventricular (RV) wall, VS, and LV posterior wall along the long axis were recorded using pulsed tissue Doppler imaging in 12 patients with constrictive pericarditis, who were diagnosed by cardiac catheterization, and also in 20 normal subjects. Peak early diastolic and atrial systolic velocities (Ew and Aw, respectively) were calculated, and the time between the aortic component of the second heart sound and the peak of the early diastolic velocity (IIA-Ew) was determined. The peak Ew and II A-Ew along the short and long axes were significantly higher and shorter, respectively, in the patient group than in the normal group. In the patient group, the motion velocity of the VS along the short axis showed a "backward" motion with a sharp and marked peak velocity immediately before Ew, or a biphasic early diastolic wave; a clear "downward" motion immediately after Ew was observed in the motion velocities of the anterior RV wall, VS, and LV posterior wall along the long axis. These distinctive backward and downward motions were not observed in any of the ventricular walls of the normal subjects. In conclusion, the early diastolic RV and LV wall motion velocity patterns along the short and long axes as measured by pulsed tissue Doppler imaging provide important information for the diagnosis of constrictive pericarditis.
OBJECTIVE: The objective of this study was to determine whether indomethacin is associated with an increased incidence of constriction of the human fetal ductus arteriosus with advancing gestational age. STUDY DESIGN: A retrospective analysis of fetal echocardiograms performed in 44 patients with premature labor or hydramnios treated with indomethacin (25 mg orally every 6 hours) was undertaken. Fisher's exact test, Kaplan-Meier survival analysis, and log-rank techniques were used; a value of p < 0.05 was considered statistically significant. RESULTS: The frequency of ductal constriction was similar for fetuses of singleton and multiple gestations. A dramatic increase in constriction was noted at 32 weeks' gestation when the rate of compromise approached 50%. CONCLUSIONS: The use of indomethacin should be restricted to gestational ages of < 32 weeks. In multiple gestations each fetus should be evaluated by echocardiography, because the ductal response may vary between individual fetuses.
The chronic constrictive pericarditis is a rare affection, with multiple etiologies and concerning especially the adult. We report a case of chronic constrictive pericarditis in an African child in whom no etiology was found. A review of the literature raises the characteristics of chronic constrictive pericarditis for a better therapeutic management.
Five patients with constriction secondary to pericarditis or membrane formation following cardiac surgical procedures are reported. In 4 of the 5 patients, a postpericardiotomy syndrome developed after the original procedure. Constriction occurred from ten weeks to almost 6 years after the cardiac operation. Clinicians should watch carefully for the delayed onset of constriction in patients with a postpericardiotomy syndrome after cardiac operation.
We present a case of an acquired constriction band caused by a tight ring on the left middle finger of a 45-year-old man. Most of the constriction band was excised and the resulting defect reconstructed with a neurovascular island flap, including a dorsal digital vein, from the adjacent ring finger. The distal end of the artery and the nerve in the flap were anastomosed and coapted to the digital artery and nerve, respectively, at the distal edge of the defect after excision of the band. The vein in the flap was anastomosed to a dorsal vein at both the distal and proximal edges of the flap as a vascularised interpositional vein graft. Four months later, the remaining constriction band was excised and the defect closed by an advancement flap. Swelling of the finger decreased and sensation improved.
Release of matrix metalloproteinases (MMP) from smooth muscle and foam cells following arterial injury facilitates cell migration, neointimal hyperplasia, and vessel wall remodeling. Inhibition of MMP activity using the hydroxamate, zinc-chelating mimicers of collagen, Batimastat and Marimastat, has shown efficacy in reducing constrictive vascular remodeling 6 weeks after experimental angioplasty but not intimal hyperplasia. Vitronectin receptor (alpha(v)beta(3)) blockade interferes with binding of this integrin to MMP-2 and proteolyzed collagen, thereby reducing cell invasion. This study tests the effect of MMP inhibition, with and without vitronectin receptor (alpha(v)beta(3)) blockade, on neointima formation and arterial remodeling in a long-term model (up to 212 months) of balloon injury in vivo. Male Sabra rats were treated with Batimastat (BB-94, British Biotech Pharmaceuticals Ltd., 30 mg/kg, intraperitoneally) and/or the alpha(v)beta(3) receptor inhibiting RGD peptide, G-Pen-GRGDSPCA (GIBCO BRL, 0.1 micromol), administered as a perivascular gel to the common carotid artery after balloon injury. Animals were sacrificed 3, 14, 25, and 75 days (n=21, 23, 22, and 21) after injury. Animals treated with BB-94, peptide, or both had markedly increased absolute luminal area with markedly reduced luminal cross-sectional-area narrowing by neointima and intima-to-media area ratio at all time points except for 3 days after balloon injury versus non-treated, ballooned animals. Combined treatment was significantly more effective than either one alone. Constrictive remodeling, most marked 212 months after balloon injury, was prevented at this time point in all treated animals. The pattern of reduction in luminal narrowing, neointimal formation, and constrictive remodeling across treatment groups correlated very significantly with the reduction in tissue MMP activity as determined by zymography at 3 days. Confirmation of the efficacy of this strategy in larger animals should be the next step toward testing the applicability of this novel approach to the interventional setting.