Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Constriction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1995

Pharmacological characterization of purinoceptor-mediated constriction of submucosal arterioles in guinea pig ileum.

Sympathetic nerve stimulation causes a constriction of submucosal arterioles that is mediated by ATP acting at P2 receptors. In the present study, we examined the P2 receptor subtype mediating this response. A computer-assisted video monitoring system measured drug-induced changes in arteriolar diameter (resting diameter approximately 40-80 microns) in pieces of submucosa in vitro. The rank-order potency for vasoconstriction caused by several ATP analogs was alpha,beta-methylene ATP (alpha,beta-MeATP) > beta,gamma-methylene ATP = 2-methylthioATP > ATP > ADP. Constrictions caused by alpha,beta-MeATP were competitively antagonized by suramin (KB = 3.2 microM) and were noncompetitively blocked by pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (KB = 0.5 microM). Norepinephrine-induced constrictions were not affected by suramin (100 microM) or by pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (3 microM). Extracellular solutions with 0 added calcium prevented constrictions caused by alpha,beta-MeATP (0.1-1.0 microM), but not those caused by norepinephrine (3 and 10 microM). Nifedipine (0.3 and 1 microM) reduced constrictions caused by 40 and 60 mM extracellular potassium chloride, but not those caused by alpha,beta MeATP. These data indicate that P2X receptors mediate constriction of submucosal arterioles. P2X-mediated vasoconstriction is dependent on extracellular calcium, but calcium entry through nifedipine-sensitive calcium channels does not contribute to P2X-mediated vasoconstriction.

Adenosine Triphosphate↗
PubMed1998

Constrictive pericarditis after coronary artery bypass surgery as a cause of unexplained dyspnea: a report of five cases.

Constrictive pericarditis after coronary artery bypass grafting (CABG) is rare and can present as unexplained dyspnea. We report five consecutive cases of post-CABG constrictive pericarditis seen within a period of 17 months at our institution. All patients presented with heart failure of unknown etiology within a period of 8-84 months after surgery. During the initial post-CABG period, two patients had developed postcardiotomy syndrome that was successfully treated with steroids. They were all assessed noninvasively and invasively. In all patients, the diagnosis of constriction was initially suspected clinically (symptoms, high jugular venous pressure with deep "X" and "Y" descents, pericardial knock). Echocardiography showed transmitral flow typical of constriction in all patients and hepatic venous flow in two. Two patients showed rapid left ventricular relaxation. In all patients, hemodynamic assessment showed diastolic equalization of pressures in all chambers, "W" shape waveform in right atrial pressure, and "dip and plateau" configuration in right and left ventricular pressure waveforms. Diagnosis was confirmed surgically in four patients who were subjected to pericardiectomy-pericardial stripping (three survived, one died). One patient refused surgery. We conclude that constrictive pericarditis, although rare, should be suspected in every case of unexplained dyspnea post CABG. It can appear early or late after surgery, and clinical examination plays an important role in its early recognition. It requires a full noninvasive and invasive assessment in case of clinical suspicion.

Aged↗
PubMed1996

Protein synthesis during regression of left ventricular hypertrophy with lisinopril in abdominal aortic constriction model of hypertension.

The use of lisinopril was assessed in inducing regression of established left ventricular hypertrophy. Left ventricular hypertrophy was achieved by aortic constriction in the rat. Lisinopril was administered in drinking water (5 mg/kg body weight/day) to aortic constricted rats starting from Day 30 for a period of further 30 days. At the end of 60 days the rates of protein synthesis were measured using the flooding dose technique. Lisinopril reduced the mixed protein contents of the regressed left ventricle from 223 +/- 7 mg to 175 +/- 10 mg/left ventricle in the aortic constricted rats; P < 0.01, all data are means +/- SEM, n = 5-8. The regression of left ventricular mass occurred along with simultaneous decrease in the rate of protein synthesis (i.e., 6.56 +/- 0.33 in aortic constricted rats versus 4.40 +/- 0.44%/day, in lisinopril treated left ventricles, P < 0.05). However, the expanded cardiocyte fiber thickness remained unchanged despite lisinopril treatment (i.e., 20.4 +/- 0.7 in aortic constricted rats versus 19.5 +/- 0.6 microm in regressed left ventricles, P > 0.05). The results indicate that regression of pressure overloaded hypertrophy with lisinopril primarily occurs by a decrease in protein synthesis in the connective tissue components of the left ventricle, although cytoskeletal components may be unaffected.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

On the elastic and rigid forms of constrictive pericarditis.

This article discusses a thesis regarding the pathophysiology of constrictive pericarditis. The thesis is that there are two forms of constriction, one being elastic and the other more analogous to a rigid shell. The two forms of constriction are considered to cause different patterns of the diagnostic signs of constriction. The elastic form is similar to cardiac tamponade, and is associated with prominent paradoxical pulse and systolic descent in the venous pressure waveform. The rigid shell type has less prominent paradoxical pulse and a more conspicuous diastolic descent in the venous pressure waveform, often associated with an early diastolic sound (pericardial knock). Recognition of these two types of constriction may be helpful in clinical diagnosis and in understanding the pathophysiology of pericardial disease.

Acute Disease↗
PubMed1989

Differentiation of constrictive pericarditis and restrictive cardiomyopathy by radionuclide ventriculography.

Patterns of left ventricular diastolic filling in five patients with unoperated constrictive pericarditis, the same five patients following pericardiectomy, five patients with restrictive cardiomyopathy, and 14 healthy control subjects were studied by radionuclide ventriculography. Patients with constrictive pericarditis had more rapid peak left ventricular filling rates (mean 5.62, range 4.23 to 7.32 end-diastolic volumes [EDV] per second) compared to control subjects 3.44, range 2.62 to 4.45 EDV/sec, p less than 0.05). Heart rate-corrected first one-third and first one-half diastolic filling fractions were greater in patients with preoperative constrictive pericarditis compared to members of the restrictive cardiomyopathy and control groups p less than 0.05). Following pericardiectomy, patients with constrictive pericarditis had significant decreases in peak filling rate and corrected filling fractions, and all diastolic filling measurements were indistinguishable from those of control subjects. These noninvasively obtained data indicate that patients with preoperative constrictive pericarditis have an increased rate of left ventricular early diastolic filling compared to patients with restrictive cardiomyopathy and control subjects, and that these findings return to normal following surgical removal of the pericardium.

Adult↗
PubMed1989

Constrictive pericarditis after cardiac surgery.

Forty-five patients were identified as having constrictive pericarditis after cardiac surgery. The mean patient age was 61 years (range, 40 to 77 years). Twenty-three of 37 patients with adequate clinical information were reported to have had a diagnosis of postpericardiotomy syndrome after the original surgery. The mean interval from original surgery to presentation with constriction was 23.4 months (range, 1 to 204 months). Computerized tomography was helpful in establishing a diagnosis of constriction in 23 of 29 patients (79%). Bypass graft patency was 93% (85 of 91 grafts). Severe pulmonary hypertension (pulmonary artery systolic pressure greater than or equal to 60 mm Hg) was present in nine patients; 8 had coexistent valvular disease (seven cases of mitral valve disease, and aortic valve disease in one). Thirty-seven of the 45 patients underwent pericardial stripping, 28 of whom experienced marked symptomatic improvement. One patient had persistent right heart failure, which was not documented to be secondary to constriction. Four patients had persistent constrictive physiologic conditions. Three of these patients had more extensive pericardial stripping and showed clinical improvement. Four patients (11%) died within 30 days of stripping. Eight patients received medical therapy alone. The decision to treat patients medically was based either on favorable response to medical therapy (five patients), or poor general clinical status.

Coronary Artery Bypass↗
PubMed1991

Constrictive pericarditis versus restrictive cardiomyopathy: a reappraisal and update of diagnostic criteria.

Distinguishing constrictive pericarditis from restrictive cardiomyopathy is a difficult clinical challenge. We review published reports in which hemodynamic criteria were used to differentiate these two diagnoses. There were 82 cases of constriction and 37 cases of restriction. The overall predictive accuracy of the difference between right and left ventricular end-diastolic pressures (RVEDP and LVEDP), RV systolic pressure, and the ratio of RVEDP to RV systolic pressure were 85%, 70%, and 76%, respectively. If all three criteria were concordant, the probability of having correctly classified the patient was greater than 90%. However, one fourth of patients could not be classified by hemodynamic criteria. There are few data to support the use of hemodynamic measurements after exercise or volume infusion to separate these two groups. Numerous recent studies have reported on the ability of left ventriculography, Doppler echocardiography, or radionuclide angiography to distinguish constriction from restriction. Many of the proposed indices appear promising, but these studies suffer from small sample size, potential selection bias, and complexity of the proposed criteria, which have limited their widespread application. New imaging technologies, such as CT scanning or MRI have been applied in a limited number of cases, but appear to be a sensitive means of detecting abnormal pericardium. Endomyocardial biopsy has proven useful in establishing the diagnosis of infiltrative cardiomyopathies, eliminating in those cases the need for surgical intervention. The finding of myocarditis must be considered a nonspecific finding that does not preclude thoracotomy. Since constrictive pericarditis is a surgically curable condition, the distinction between constrictive and restrictive disease is of critical importance. Taking into account the relative contribution of data derived from hemodynamic, imaging,and biopsy studies, we propose an algorithm for the selection of appropriate candidates for pericardial biopsy and stripping.

Algorithms↗
PubMed1978

Echocardiography: pericardial thickening and constrictive pericarditis.

A total of 167 patients with pericardial thickening noted on M node echocardiography were studied retrospectively. After the echocardiogram, 72 patients underwent cardiac surgery, cardiac catheterization or autopsy for various heart diseases; 96 patients had none of these procedures. In 49 patients the pericardium was directly visualized at surgery or autopsy; 76 percent of these had pericardial thickening or adhesions. In another 8 percent, pericardial adhesions were absent, but no comment had been made about the appearance of the pericardium itself. In the remaining 16 percent, no comment had been made about the pericardium or percardial space. Cardiac catheterization in 64 patients revealed 24 with hemodynamic findings of constrictive pericarditis or effusive constrictive disease. Seven echocardiographic patterns consistent with pericardial adhesions or pericardial thickening are described and related when possible to the subsequent findings at heart surgery or autopsy. The clinical diagnoses of 167 patients with pericardial thickening are presented. The hemodynamic diagnosis of constrictive pericardial disease was associated with the echocardiographic finding of pericardial thickening, but there were no consistent echocardiographic patterns of pericardial thickening diagnostic of constriction. However, certain other echocardiographic abnormalities of left ventricular posterior wall motion and interventricular septal motion and a high E-Fo slope were suggestive of constriction.

Echocardiography↗
PubMed1980

Genesis of pericardial knock in constrictive pericarditis.

A pericardial knock is a common finding in constrictive pericarditis. However, its origin has been uncertain. One hypothesis suggests that it is due to sudden deceleration of ventricular filling. To validate this hypothesis, left ventriculograms, phonocardiograms and external pulse recordings were obtained in seven patients with hemodynamic and pathologic findings of constrictive pericarditis and in seven normal subjects. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume versus diastolic filling time were constructed for each patient. Pericardial knock was recognized as an early high frequency sound recorded between 90 to 120 ms after the aortic closing sound and occurring at the trough of the Y descent of the jugular venous pressure tracing. The timing of the pericardial knock in five patients with constrictive pericarditis corresponded to a sudden and premature plateau of the diastolic left ventricular volume curve representing 85 +/- 4 percent (mean +/- standard deviation) of ventricular filling. The diastolic plateau was missing in two patients with constrictive pericarditis who had no pericardial knock. In these cases, the rate of ventricular filling was faster than normal in the first 20 percent of diastole. Thus, this study related pericardial knock to an abrupt plateau inthe diastolic left ventricular volume curve, supporting the view that sudden cessatin of ventricular filling generates the pericardial knock of constrictive pericarditis. Two mechanisms are proposed by which the filling plateau may produce the knock, and it is postulated that both ventricles may participate in the knock phenomenon.

Adult↗
PubMed1982

Constrictive pericarditis as a complication of cardiac surgery: recognition of an entity.

Among 5,207 adult patients who underwent cardiac surgery, postoperative constrictive pericarditis was recognized in 11 patients (0.2% incidence rate). Seven patients had coronary arterial bypass grafting and 4 had valve replacement; the pericardium was left open in all cases. The average interval between surgery and presentation of pericardial constriction was 82 days (range 14 to 186). M mode echocardiography revealed epicardial and pericardial thickening in 7 cases and variable degrees of posterior pericardial effusion in 5 cases. Cardiac catheterization demonstrated uniformity of diastolic pressures with a characteristic early diastolic dip and late plateau pattern. Two patients responded to medical therapy for chronic pericarditis. One patient had a limited parietal pericardiectomy followed by recurrent constrictive pericarditis that eventually stabilized with medical therapy. The other 8 patients required radical pericardiectomy. The pathophysiology of constriction after surgery is unclear. Its clinical expression involves a wide spectrum of presentation and therapeutic response. Constrictive pericarditis may be a complication of cardiac surgery in spite of an open pericardium and should be considered in postoperative patients who present with deteriorating cardiac function.

Adrenal Cortex Hormones↗
PubMed1987

Transient cardiac constriction: an unrecognized pattern of evolution in effusive acute idiopathic pericarditis.

In 16 of 177 patients with effusive acute idiopathic pericarditis (10 men, 6 women, mean age 38 years), features of cardiac constriction were detected (by physical examination in 6 patients and by noninvasive recordings in all) between 5 and 30 days after an echocardiogram had shown pericardial effusion, at a time when signs of activity had abated and effusion was already minimal or had altogether disappeared. Cardiac catheterization was performed in 5 patients, showing either overt (3 patients) or occult (2 patients) cardiac constriction. Two patients had clinical signs of cardiac failure. After a mean of 2.7 months, the features of constriction had spontaneously disappeared in all patients in the clinical examination and noninvasive recordings, and remained so in subsequent control studies (mean follow-up 31 months). Repeat cardiac catheterization in the 5 patients in whom it had been previously performed showed normal features both in the basal state and after fluid overload. The results of the present study show that some patients may go through a transient phase of cardiac constriction at the end of the effusive period of acute idiopathic pericarditis. Features of constriction are, in most cases, subtle and can go unrecognized if not specifically sought. However, they may have clinical relevance in some patients. These findings provide insight into the resolution phase of effusive acute idiopathic pericarditis, and an unnecessary pericardiectomy may be avoided.

Acute Disease↗
PubMed1993

Rate-dependent hemodynamic responses during incremental atrial pacing in chronic constrictive pericarditis before and after surgery.

Chronic constrictive pericarditis is a frequent cause of diastolic dysfunction, and results in impaired ventricular filling. Unlike in normal subjects, ventricular filling in constrictive pericarditis occurs almost entirely in the initial one third of diastole, and cardiac output is dependent predominantly on heart rate. Tachycardia impairs ventricular filling in normal subjects, but its effects in patients with constrictive pericarditis have not been studied. The effect of increasing heart rate alone with atrial pacing on the central and peripheral hemodynamics of patients with untreated chronic constrictive pericarditis before and after pericardiectomy was evaluated. Increased heart rate with atrial pacing increased cardiac output, whereas stroke volume remained unchanged up to heart rates of 140 beats/min. Further increases in heart rate resulted in reductions of cardiac output and stroke volume. There were no significant changes in ventricular filling pressures. Infusion of 300 ml of saline solution at peak pacing rates did not improve cardiac output. After successful surgical pericardiectomy, the hemodynamic effects of atrial pacing returned to normal. It is concluded that moderate tachycardia improves the hemodynamic profile of patients with constrictive pericarditis.

Adult↗
PubMed1985

Some effects of prolonged constriction on nerve regeneration in the rabbit.

Serial nerve conduction studies have been used to study the time-course of regeneration after tibial nerve crush in the rabbit, and the effect on this of a constricting ligature 5 mm distal to the site of crush. Transverse sections from the region of the ligature showed that when constriction was severe, the regenerating fibers had difficulty in penetrating the constricted region, and that some took an aberrant course in superficial connective tissue outside the ligature. In 2 out of 6 animals no fibres succeeded in passing through the centre of ligature, but aberrant fibres were able to re-enter distal fascicles and to reinnervate distal muscles. When compared with findings after crush alone, the time taken to reinnervate distal muscles was increased by a ligature, and distal fibre diameter and motor conduction velocity remained low. Low voltage, long-duration, polyphasic muscle action potentials were evoked by distal nerve stimulation, and axon reflexes suggested excessive axon branching within nerve trunks. Since these changes were seen in the distal parts of both constricted and aberrant fibres, they cannot be attributed to constriction alone. Similar changes might be expected in other peripheral nerve lesions in which loss of fascicular continuity and neuroma formation occur.

Animals↗
PubMed1990

Myocardial and endocardial involvement in tuberculous constrictive pericarditis: difficulty in biopsy distinction from endomyocardial fibrosis as a cause of restrictive heart disease.

Differentiation of constrictive pericarditis and endomyocardial fibrosis by the available diagnostic methods is difficult at present. With this in mind, we compared autopsy data in heart specimens from 8 patients of constrictive pericarditis of tuberculous origin and 6 patients with tropical endomyocardial fibrosis. Post-mortem endomyocardial biopsies were also performed from both the ventricles. Pericardial thickening and adhesions were present in all cases of constrictive pericarditis and in none of those with endomyocardial fibrosis. Interestingly, significant endocardial thickening was seen in four, and myonecrosis, lymphohistiocytic cellular infiltration and myofibrosis were observed in seven of the eight cases of constrictive pericarditis. This suggests that the tubercular insult to heart may result in involvement of all three layers with varying severity. The endomyocardial biopsy specimens from the affected areas revealed similar histopathological changes of endocardial thickening and focal myofibrosis with cellular infiltrates in patients with both constrictive pericarditis and endomyocardial fibrosis, making distinction of the two difficult. The hallmark of differentiation between these two clinical entities appears to be a diligent attempt at identification of the thickened pericardium.

Biopsy↗
PubMed1993

Poor outcome in radiation-induced constrictive pericarditis.

PURPOSE: To compare the outcome of patients with radiation-induced constrictive pericarditis versus patients with constriction due to another etiology. METHODS AND MATERIALS: Twenty patients with constrictive pericarditis seen during 1975-1986 at a single medical center. Six had radiation-induced constrictive pericarditis (Group A). The etiology was idiopathic in ten subjects and secondary to carcinomatous encasement, chronic renal failure, purulent infection and tuberculosis in one patient each (Group B, N = 14). Mean age was 53.4 +/- 15.5 years. RESULTS: Extensive pericardiectomy was performed in 3/6 Group A and 13/14 Group B patients. All Group A patients died, 4 weeks--11 years post-diagnosis (median = 10 months). Two Group A patients died suddenly, one died post-operatively of respiratory failure, another of pneumonia and two of recurrent carcinoma. Thirteen Group B patients are alive (median follow-up = 72 months). The only death in this group was due to metastatic cancer. CONCLUSION: The poor outcome with radiation-induced constriction is probably multi-factorial. Poor surgical outcome is to be expected in patients with evidence of recurrent tumor, high-dose irradiation, pulmonary fibrosis or associated radiation-induced myocardial, valvular or coronary damage.

Adult↗
PubMed2004

Transient constrictive pericarditis: causes and natural history.

OBJECTIVES: This study was designed to elucidate the causes and natural history of transient constrictive pericarditis (CP). BACKGROUND: In some patients with acute CP, the symptoms and constrictive physiologic features resolve with medical therapy alone, a phenomenon that has been labeled "transient constrictive pericarditis." No large studies have examined the causes or natural history of transient CP. METHOD: Review of the Mayo Clinic echocardiogram database identified 212 patients who had echocardiographic findings of CP from 1988 through 1999. Demographic, clinical, and echocardiographic findings were identified in all patients. In 36 of these patients, follow-up echocardiograms showed resolution of the constrictive hemodynamics without pericardiectomy. RESULTS: The average age of the patients was 49 +/- 21 years, and 72% were men. The causes for the CP were diverse, the most common being prior cardiovascular surgery (25%). In a subset of 22 patients who were followed serially during the course of their illness, resolution of the constrictive physiologic features occurred at an average of 8.3 weeks after diagnosis. CONCLUSIONS: A subset of patients with CP experience resolution of the disorder without requiring pericardiectomy.

Adolescent↗
PubMed1996

Magnetic resonance imaging of pericardial constriction: comparison of cine MR angiography and spin-echo techniques.

AIM: Spin-echo (SE) MRI detects pericardial thickening in pericardial constriction but the validity of extrapolating SE criteria to cine MRA imaging has not been tested. Pericardial thickness measured by SE and cine MRA was compared in patients with and without pericardial thickening to determine if the range of pericardial thickness measured by the two techniques is the same. PATIENT AND METHODS: Fourteen patients, investigated for possible pericardial constriction (PC), were compared with 24 subjects without evidence of pericardial disease (controls). Images were acquired using SE and cine MRA. Pericardial thickness was compared with final diagnosis. RESULTS: Pericardial thickening ( > 3.5 mm) by SE detected pericardial constriction: sensitivity = 100% specificity = 96%, kappa = 0.91. Cine MRA had a sensitivity = 86%, specificity = 63%, kappa = 0.33. Maximum differences between SE and cine MRA pericardial thickness ranged from +2.5 mm to -2/7 mm. CONCLUSIONS: Spin-echo identifies pericardial thickening with little overlap between measurements in patients with and without pericardial constriction. Pericardial thickness on cine MRA usually exceeds SE thickness, but with considerable overlap of thickness measurements in patients with and without pericardial constriction. Cine MRA cannot be used alone to diagnose pericardial thickening.

Diagnosis, Differential↗
PubMed1983

Atrial systolic notch on the interventricular septal echogram: an echocardiographic sign of constrictive pericarditis.

Interventricular septal motion during ventricular diastole was analyzed using M-mode echocardiography in 13 patients with constrictive pericarditis and 12 patients with restrictive cardiomyopathy. In seven of eight patients with constrictive pericarditis in sinus rhythm, an abnormal "atrial systolic" notch was observed consisting of abrupt initial posterior motion toward the left ventricle approximately at the middle of the P wave and subsequent anterior motion at the end of the P wave and termination before the R wave. This notch was absent during atrial premature beats that were recorded in two patients. The atrial systolic notch was not observed in any patient with restrictive cardiomyopathy. The septal notch in early ventricular diastole previously described in constrictive pericarditis was seen in 62% of patients with constrictive pericarditis and 25% of patients with restrictive cardiomyopathy. Thus, an abnormal atrial systolic notch may be an additional useful sign to differentiate constrictive pericarditis from restrictive cardiomyopathy. The mechanism may be related to transient late diastolic pressure gradients between both ventricles resulting from asynchrony of left and right atrial contractions.

Diastole↗