Murmur Of Mitral Regurgitation Research Articles

The relationship of carditis to the initial attack of Sydenham's chorea

Background: The natural history of valvular regurgitation detected by echocardiography in Sydenham's chorea has been lacking. Methods: Clinical assessment and transthoracic color Doppler echocardiography were independently performed for each patient with an initial attack of Sydenham's chorea and also for each normal control (Khon Kaen University, Thailand; 1991–2001) at the time of their presentations. Serial clinical examinations and echocardiography were done for each patient at 1- and at 5-year follow-up. Results: Of 44 patients, 17 (39%) had carditis (valvulitis) evident by auscultation at the time of the initial attack. Three (11%) of the 27 patients with no clinical evidence of carditis had echocardiographic evidence of acute mitral regurgitation (subclinical valvulitis). All 17 patients with carditis had echocardiographic evidence of acute mitral regurgitation. None of the 88 control children had evidence of pathologically significant valvular regurgitation. Of the 15 patients with carditis regularly followed, the persistence of a mitral regurgitation murmur and of pathologically significant valvular regurgitation by echocardiography were 33% (5/15) and 60% (9/15), respectively, at 1-year follow-up, but the persistence of both was 25% (1/4) at 5-year follow-up. Conclusions: Color Doppler echocardiography is a useful tool in the early diagnosis of rheumatic carditis (valvulitis) and at 1-year follow-up of rheumatic valvular heart disease in the patients with initial Sydenham's chorea but the incremental benefit beyond 5 years after the initial attack might be minimal.

Reversible Mitral Valve Prolapse and Mitral Regurgitation in Children with Graves' Disease

An association between mitral valve prolapse (MVP) and hyperthyroidism has been described in adults. However, the long-term prognosis when associated with significant mitral regurgitation remains unclear. Three consecutive children with Graves' disease were found to have a loud mitral regurgitation murmur (grade III/VI) and echocardiographic evidence of MVP with moderate mitral regurgitation. The cardiac manifestations included palpitations, exertional dyspnea, and exercise intolerance. The electrocardiograms at presentation were sinus tachycardia in all cases. All had hyperthyroidism and positive thyroid antibodies. Exophthalmos occurred in two and appeared later than the cardiac symptoms in one. The cardiac murmur disappeared in all patients when antithyroid agents controlled the hyperthyroidism. Follow-up echocardiography showed normal in one and MVP with mild mitral regurgitation in two. We conclude that MVP and significant mitral regurgitation can occur in children with hyperthyroidism, especially those with Graves' disease. The prognosis is good after adequate medical control of the hyperthyroidism.

Subclinical rheumatic valvitis: a long-term follow-up

In order prospectively to investigate the frequency and evolution of subclinical valvitis, we selected 40 consecutive patients suffering their initial attack of rheumatic fever, seen in our clinic from 1992 to 1994, and followed-up until 2001, with a mean period of follow-up of 8.1 years, and a standard deviation of 0.6 year. We also assembled a matched control group of 37 healthy children and adolescents. We discovered a murmur of mitral regurgitation in 28 (70.0%) of the patients. In 3 (7.5%) of these patients, there was also a murmur of aortic regurgitation. In the group of 28 symptomatic patients, Doppler echocardiography showed mitral regurgitation in all, and aortic regurgitation in 17. In the group of 12 patients without clinical evidence of cardiac involvement, Doppler echocardiography identified mitral regurgitation in 2, isolated in one and associated with aortic regurgitation in the other. Thus, the frequency of subclinical valvitis was 16.7%. In patients with subclinical valvitis only the aortic regurgitation regressed during the period of follow-up. In the group of 28 symptomatic patients, mitral regurgitation disappeared in 6 (21.4%), aortic regurgitation in 7 of the 17 having this feature (41.2%), while 2 patients (7.1%) developed mitral stenosis. The sensitivity and specificity of cardiac auscultation were, respectively, 93.3%, with 95% confidence intervals between 72.3% and 97.4%, and 100%, with 95% confidence intervals between 65.5% and 100%, for the diagnosis of mitral regurgitation, and 16.7%, with 95% confidence intervals between 4.4% and 42.3%, and 100%, with 95% confidence intervals between 81.5% and 100%, for that of aortic regurgitation. We conclude that the Doppler echocardiogram is an important means of diagnosing and assessing the evolution of subclinical rheumatic valvar lesions, which are not always transient. We suggest that Doppler echocardiography should be performed in all patients with acute rheumatic fever. Subclinical valvitis should be considered as mild carditis, provided that strict criterions are observed in the differential diagnosis from physiological regurgitation, and Doppler echocardiographic findings are analyzed in the context of the other manifestations of the disease.

Evaluation and Management of a Patient With Congestive Heart Failure

A 44-year-old woman initially presented to her primary physician in April 1998 with a cough and dyspnea that had persisted for about 1 month. A chest roentgenogram demonstrated clear lungs but a “globular” cardiac configuration. She was given therapy with amoxicillin combined with clavulanate potassium (Augmentin; GlaxoSmithKline; Research Triangle Park, NC) for 1 week with apparent diminution of the severity of the dyspnea. After feeling fairly well for 1 month, she began experiencing cough, dyspnea, chest pressure, and extreme fatigue. The dyspnea resulted from minimal activity and was associated with orthopnea. The patient’s medical history was unrevealing. Specifically, there was no evidence of prior coronary artery disease (CAD), hypertension, heavy alcohol intake, or recent pregnancy. She then was referred to a cardiologist and was found to have a BP of 100/70 mm Hg, sinus tachycardia at 120 beats/min, and no evidence of jugular venous distension or peripheral edema. A cardiac examination disclosed an apical impulse displaced 2-cm lateral to the midclavicular line, a prominent third heart sound, and a grade 2/6 apical systolic murmur of mitral regurgitation. A chest roentgenogram again demonstrated cardiomegaly with clear lung fields. An echocardiogram disclosed a moderately dilated left ventricle with normal wall thickness and severe global hypokinesis (estimated ejection fraction, 20 to 25%), which is indicative of generalized dilated cardiomyopathy. The left atrium was mildly dilated, and the right heart chambers were normal in size and motion. The patient then was admitted to the hospital and received therapy with digoxin, diuretics, and a lowdose angiotensin-converting enzyme (ACE) inhibitor. Her symptoms gradually improved.

Mechanism of spontaneous diminution of mitral regurgitation following percutaneous mitral valvuloplasty with the Inoue balloon

To the Editor: stepwise technique of PBMV with the Inoue balloon [7,8] I agree with Krishnamoorthy et al. [1] that most patients with mitral regurgitation (MR) following percutaneous balloon mitral valvuloplasty (PBMV) with the Inoue balloon showed gradual improvement in their MR and symptoms. My colleagues in China and I [2] reported in 1995 the largest series of patients who underwent PBMV with the Inoue balloon technique. Among 4832 patients, 1.4% developed severe MR (z 3+/4+); emergency mitral valve replacement was performed in 6 patients and elective mitral valve replacement in 12; in most of the patients the preexisting MR did not show any significant change after PBMV [2]. The production of or increase in MR that followed PBMV improved in more than half of the patients at follow-up catheterization [3–5]. Four mechanisms have been postulated: (1) reversible mitral valve stretching by PBMV; (2) better leaflet coaptation following balloon dilation of the stenotic mitral valve; (3) fibrosis and healing of the end of the commissures which may diminish MR resulting from excessive commissural splitting; and (4) improvement in transient papillary muscle dysfunction caused by balloon trauma to the papillary muscles at the time of PBMV [6]. Therefore I always advise watchful waiting in managing mild to moderate MR that followed PBMV with the Inoue balloon. The MR murmur in many of these patients diminished in intensity, or even disappeared, over the follow-up period. Clinically they remained much improved. If the

An assessment of the terminology used by diplomates and students to describe the character of equine mitral and aortic valve regurgitant murmurs: correlations with the physical properties of the sounds.

Twenty students and 16 diplomates listened to 7 recordings made from 7 horses with either aortic (n = 3) or mitral valve (n = 4) regurgitant murmurs. A total of 30 different terms were used to describe the character of these murmurs. However, only 4 terms were used in a repeatable and consistent manner. Most people described the character of a given mitral or aortic valve murmur with 1 or 2 terms. Diplomates drew from a pool of terms that was about half the size of that used by students--8.1 +/- 2.0 terms for diplomats (mean +/- 1 SD) versus 13.1 +/- 1.8 terms for students (P > .001). Only blowing, honking, buzzing, and musical were markedly associated with the recording played. Frequency analysis of the murmurs allowed them to be classified as containing harmonics (n = 4) or not containing harmonics (n = 3). Blowing was used to describe murmurs without harmonics on 39 of 48 occasions and corresponds to the term noisy used in some older descriptions of equine murmurs. Honking, musical, and buzzing were markedly associated with murmurs that contained harmonics; these terms were used 23, 13, and 12 of a possible 64 times, respectively. The frequency of buzzing and honking murmurs (72.7 +/- 9.3 and 88.4 +/- 46.3 Hz, respectively) was markedly lower than that of musical murmurs (156.8 +/- 81.1 Hz) (all P values < .01). Honking murmurs (0.392 +/- 0.092 seconds) were shorter than those described as buzzing or musical (0.496 +/- 0.205 and 0.504 +/- 0.116 seconds, respectively). The data suggest that the terminology for the character of aortic and mitral regurgitant murmurs should be restricted to 4 terms: blowing, honking, buzzing, and musical. Honking, buzzing, and musical describe murmurs with a peak dominant frequency and harmonics; blowing describes murmurs without a peak frequency. Effective communication could be enhanced by playing examples of reference sounds when these terms are taught so that nomenclature is used more uniformly.

An Assessment of the Terminology Used by Diplomates and Students to Describe the Character of Equine Mitral and Aortic Valve Regurgitant Murmurs: Correlations with the Physical Properties of the Sounds

An Assessment of the Terminology Used by Diplomates and Students to Describe the Character of Equine Mitral and Aortic Valve Regurgitant Murmurs: Correlations with the Physical Properties of the Sounds

Effect of age and training on murmurs of atrioventricular valvular regurgitation in young thoroughbreds.

Cardiac auscultation was carried out on 111 Thoroughbred horses age 2-5 years to test the hypothesis that athletic training might influence the development of atrioventricular (AV) valve regurgitation in young Thoroughbreds. Murmurs of valvular regurgitation were identified and graded on a 1-6 scale. There were 2 sources of auscultation data: 1) 55 2-year-old horses that were examined by auscultation before training commenced and 9 months later when at race fitness; 2) 56 horses age 2-5 years that were examined on one occasion only (25 2-year-olds, 23 3-year-olds, five 4-year-olds and five 5-year olds). All horses in the second data set were in full training and racing regularly at the time of the examination. To conclude the study, 35 horses were selected randomly from both groups of horses and examined with colour-flow Doppler echocardiography. The aim of the final part of the study was to check specificity and sensitivity of auscultation for detection of AV valve murmurs and therefore validate the auscultation findings. Prior to training, the prevalence in 2-year-old racehorses of murmurs of mitral regurgitation and tricuspid regurgitation was 7.3% (4/55) and 12.7% (7/55), respectively. After training, the prevalence proportions increased to 21.8% (12/55) and 25.5% (14/55). After training, one horse developed a murmur characteristic of aortic regurgitation. The differences in murmur prevalence were statistically significant for mitral and tricuspid regurgitation (paired t test results: mitral regurgitation, P = 0.019; tricuspid regurgitation, P = 0.007), as were the differences in mean murmur grade (P = 0.018 and P = 0.0006, respectively). There were no significant effects of age on the prevalence of valvular regurgitation in 56 horses examined at race fitness. Auscultation was a specific (specificity 100%) and reasonably sensitive method for detection of murmurs of mitral and tricuspid regurgitation (mitral regurgitation: positive predictive value 100%, negative predictive value 84%, tricuspid regurgitation: positive predictive value 100%, negative predictive value 65%). These data suggest that the prevalence and grade of murmurs of mitral and tricuspid valvular regurgitation increase in 2-year-old Thoroughbreds after 9 months of athletic training. Whereas the effects of age and growth on the prevalence of murmurs cannot be ruled out from these data, this study suggests that there is an influence of athletic training on the development of atrioventricular valvular regurgitation in flat-racing Thoroughbreds.

Anomalous origin of the left coronary artery from the right pulmonary artery with intramural aortic trajectory. Clinicosurgical diagnostic implications.

Anomalous origin of the left coronary artery from the right pulmonary artery (AOLCARPA), is a rare entity that is usually associated with other defects. Of the 20 cases of AOLCARPA reported in the literature, 14 (70%) had associations. We describe four patients with AOLCARPA without associated defects, but with a peculiar intramural aortic trajectory. Fifty-five patients with anomalous origin of the left coronary artery were operated upon at INCORFMUSP. Four of the patients had the anomalous origin from the right pulmonary artery (RPA) without associated defects but with intramural aortic trajectory. Clinical and laboratory examinations were analyzed, as well as surgical findings. All patients had congestive heart failure (CHF) and 3 also had angina pectoris. Two patients had a murmur of mitral regurgitation, signs of myocardial infarction on the ECG and cardiomegaly. The shortening fraction varied from 9% to 23%. The hemodynamic study confirmed the diagnosis of anomalous origin of the coronary artery, but the intramural trajectory and the origin from the RPA were established only at surgery. In 3 patients, the technique of side-to-side anastomosis was performed with a good outcome. One patient, who underwent end-to-side anastomosis, died 6 months after the surgery. Association with other defects usually occurs in the AOLCARPA, and the intramural aortic trajectory is difficult to clinically diagnose but easy to surgically correct.

Effects of Dobutamine Infusion on Mitral Regurgitation.

Both intensity of mitral regurgitant murmur and color-coded Doppler regurgitant signal area have been reported to correlate with the degree of regurgitation. To evaluate the relationship between the intensity of regurgitant murmur and severity of mitral regurgitation, phonocardiography, echocardiography, and Doppler ultrasound were performed in 18 patients with mitral regurgitation before and during dobutamine infusion. Mitral regurgitation was due to mitral valve prolapse with ruptured chordae tendineae in 8 patients, rheumatic change in 5 patients, and dilated cardiomyopathy in 5 patients. With intravenous dobutamine infusion, heart rate (77-103 beats/min), systolic blood pressure (119-144 mmHg), peak mitral regurgitant jet velocity (4.5-5.4 m/sec), intensity of mitral regurgitant murmur (to 201% of that before infusion in early systole) increased, while left ventricular end-diastolic volume (124-102 mm), left ventricular end-systolic volume (57-42 mm), mitral anular diameter (33-28 mm), and color Doppler mitral regurgitant signal area (704-416 mm(2)) decreased (P < 0.05). Total (forward + backward) left ventricular stroke volume (66-61 mL/beat) showed no change. Dobutamine decreased mitral regurgitant flow/beat, regardless of etiology of mitral regurgitation, which was probably due to the decrease of left ventricular size and mitral annular diameter. Although total (forward + backward) left ventricular stroke volume was unchanged, dobutamine effectively increased forward left ventricular stroke volume by decreasing backward regurgitation. Mitral regurgitant murmur became louder despite the decrease of mitral regurgation, indicating the uselessness of auscultation in the grading of the severity of mitral regurgitation.

Doppler echocardiography distinguishes between physiologic and pathologic "silent" mitral regurgitation in patients with rheumatic fever.

The diagnosis of rheumatic fever is based on physical findings (major) and supporting laboratory evidence (minor) as defined by the Jones criteria. Rheumatic carditis is characterized by auscultation of a mitral regurgitant murmur. Doppler echocardiography, however, may detect mitral regurgitation when there is no murmur ("silent" mitral regurgitation), even in normal individuals. The hypothesis of this study was that physiologic mitral regurgitation can be differentiated from pathologic "silent" mitral regurgitation by Doppler echocardiography. The study group consisted of 68 patients (2-27 years) with normal two-dimensional imaging and Doppler evidence of mitral regurgitation but no murmur. Patients with rheumatic fever (n = 37) met Jones criteria (chorea in 20, arthritis in 17). Patients without rheumatic fever (n = 31) were referred for innocent murmur (n = 7), abnormal electrocardiogram (n = 13), and chest pain (n = 11). Echoes were independently reviewed by two cardiologists blinded to the diagnosis. Pathologic mitral regurgitation was defined as meeting the following four criteria: (1) length of color jet > 1 cm, (2) color jet identified in at least two planes, (3) mosaic color jet, and (4) persistence of the jet throughout systole. Jet orientation was also noted. Using the above criteria, there was agreement in echo interpretation of pathologic versus physiologic mitral regurgitation in 67 of 68 patients (interobserver variability of 1.5%). Pathologic regurgitation was found in 25 (68%) patients with rheumatic fever but in only 2 (6.5%) patients without rheumatic fever (p < 0.001). The specificity of Doppler for detecting pathologic regurgitation was 94% with a positive predictive value of 93%. The color mitral regurgitant jet was posteriorly directed in all 25 patients with rheumatic fever. Pathologic "silent" mitral regurgitation of rheumatic fever can be distinguished from physiologic mitral regurgitation using strict Doppler criteria, particularly when the jet is directed posteriorly. These data support the use of Doppler echocardiography as a minor criterion for evaluating patients with suspected rheumatic fever.

Unstable Angina: Are We Able to Recognize High-Risk Patients?

It is difficult to identify characteristics of patients with unstable angina that are predictive of a high likelihood of developing clinical events. However, several features have been recognized. Patients with a clinical history of previous stable exertional angina symptoms who began to experience rest pain appear to be at risk and tend to have more extensively underlying coronary disease. When the ischemic episodes are accompanied by rates, a new or worsening mitral regurgitation murmur, or hypotension, there is a high likelihood of significant coronary artery disease and one should triage these patients to early cardiac catheterization and prompt revascularization. An angiographic feature that carries a high risk is a lesion in the proximal left anterior descending or in the left main coronary artery. Certain typical ECG patterns are very suggestive for a critical narrowing in these coronary arteries. If chest pain and ST-segment changes recur on vigorous medical management, early invasive evaluation should be strongly considered. Even so, the left ventricular function is very important prognostically. According to serologic tests, the level of C-reactive protein and serum amyloid A protein suggesting that there may be active inflammation predicts an early poor outcome. However, these serologic abnormalities do not have much clinical value. An increased platelet activation and a reduced fibrinolytic capacity play a role in the pathogenesis of unstable angina, but thrombolytic therapy does not improve the prognosis in patients with unstable angina.

Clinical significance of the apical late systolic ejection murmur: a new phonocardiographic sign indicating dynamic mid-left ventricular obstruction.

Systolic ejection murmurs of the left heart usually have their peak during early to mid-systole. Few reports have addressed ejection murmurs with their peak at late systole. We evaluated the clinical significance of an apical systolic ejection murmur with a peak intensity during late systole using Doppler and two-dimensional (2-D) echocardiography and phonocardiography. The apical late systolic ejection murmur was observed in 9 of 13 consecutive patients with mid-left ventricular obstruction. We investigated the ejection flow velocity and the timing of maximum velocity at the three different sites of the left ventricle, the left ventricular cavity shape, and the timing of the peak murmur intensity in these nine patients (late-murmur group). The same parameters were also examined in 8 consecutive patients with mid-systolic ejection murmurs (mid-murmur group), 10 with early systolic ejection murmurs (early-murmur group), and 7 controls without murmurs. Patients with aortic stenosis were excluded. The mid-ventricular ejection flow velocity was significantly higher in the late-murmur group than in the other three groups; that of the outflow tract was markedly higher in the mid-murmur group. The ejection flow velocity at the aortic orifice of patients in the early-murmur group was significantly high compared with that of the controls. The timing of the peak murmur intensity in each group correlated with that of the peak flow signal at the corresponding site with maximum velocity. In all patients in the late-murmur group, 2-D echocardiography revealed a systolic narrowing of the cavity at the mid-ventricle. Amyl nitrite inhalation induced a marked increase in the intensity of the murmur without evidence of appearing or increasing mitral regurgitation. It was concluded that the apical ejection murmur with a late systolic peak intensity is a new phonocardiographic sign indicative of dynamic, mid-left ventricular obstruction. This murmur should be differentiated from the mitral regurgitant murmur.

Reversibility of mitral regurgitation following rheumatic fever: clinical profile and echocardiographic evaluation.

The clinical disappearance of the murmur of rheumatic mitral regurgitation after period of time has been documented by many researchers. However no studies have related the disappearance of the murmur with the functional or anatomical state of the mitral valve. This study was done to elucidate the mitral valve status using doppler and color coded echocardiography among those children who have lost their apical pansystolic murmur on auscultation following a documented attack of rheumatic fever. The study sample consisted of 51 patients including 31 patients in whom the murmur has disappeared (group I), and 20 patients with persistent isolated mitral regurgitation (group II). Patients of group I had significantly lower grades of murmur intensity, lower incidence of cardiomegaly, and had no heart failure in the initial attack. They were more compliant with prophylaxis and had less recurrences than patients of group II. The murmur disappeared in patients of group I from 1/2 to 14 years after the initial attack. Echocardiography revealed that such patients had a normal mitral valve apparatus, and a normal heart size and function. Only 5 patients of this group had a significant regurgitant jet demonstrated by colour doppler. We concluded that recovery of the mitral valve and return of cardiac functions to normal is possible in patients who had mitral regurgitation following rheumatic fever. Some of them may still have an inaudible mild regurgitation. Patients who have lost their murmur may be allowed to exercise freely, yet penicillin prophylaxis should not be discontinued.

Recent developments in the diagnosis and management of mitral valve prolapse.

Mitral valve prolapse (MVP), which occurs in about 3% of adults, is usually a primary, dominantly inherited condition. MVP may be diagnosed by auscultation of a mid-systolic click and late-systolic murmur that move dynamically with postural maneuvers. M-mode echocardiography confirms MVP by demonstrating late-systolic prolapse and two-dimensional echocardiography reveals leaflet billowing into the left atrium. Echocardiography identifies severe forms of MVP by documenting significant mitral regurgitation, enlargement and thickening of the mitral leaflets and annulus, and loss of leaflet apposition. In contrast to early reports, true "MVP syndrome" as revealed by controlled studies consists of low body weight and blood pressure, minor skeletal abnormalities, orthostatic hypotension, palpitations, and mitral regurgitation that is usually mild. Complications of MVP include progressive mitral regurgitation, infective endocarditis, orthostatic syncope, and possible risks of neurologic ischemia and arrhythmic sudden death. Risk factors we have identified for complications among patients with MVP include older age, male gender, the presence of mitral regurgitation, and possibly, higher weight and blood pressure. The cumulative risk of all complications of MVP by age 75 is from 5% to 10% for affected men and 2% to 5% for affected women. Patients with MVP who have neither a murmur nor Doppler evidence of mitral regurgitation may be reassured that their condition is benign. For other patients with MVP we have shown that oral antibiotic prophylaxis is cost-effective. The presence and severity of mitral regurgitation govern the frequency and intensiveness of follow-up.

Some Familiar Trade-offs

Stage A 77-year-old man with mitral-valve prolapse said he had had insomnia and shortness of breath for five days. A murmur of mitral regurgitation had first been noted nine years earlier. Response The patient's mitral regurgitation could have progressed, producing congestive heart failure, but in an elderly man coronary artery disease and a myocardial infarction would surely be possible. I wonder if the patient is a smoker with chronic pulmonary disease. He could have pneumonia, but I would put congestive heart failure first on my list. Stage He was short of breath when walking across the room, but he had . . .

Mitral regurgitation in early myocardial infarction. Incidence, clinical detection, and prognostic implications. TIMI Study Group.

To investigate mitral regurgitation occurring early in the course of acute myocardial infarction with respect to its incidence, the impact of infarct size and location, the accuracy of clinical detection, the contribution of global and regional left ventricular performance, and its influence on prognosis. Prospective observational study derived from patients entering Phase I of the Thrombolysis in Myocardial Infarction (TIMI) trial. Multicenter trial involving 13 university-affiliated medical centers. A total of 206 patients studied within 7 hours of symptom onset during their first myocardial infarction. Contrast left ventriculography was used to document mitral regurgitation. Mitral regurgitation was present in 27 patients (13%). Although the presence of regurgitation correlated with the site of infarction (20 of 27 had anterior infarctions) and the number of akinetic chords, it was not statistically related to the peak creatine kinase value or to left ventricular chamber size or filling pressure. A murmur of mitral regurgitation was heard in only 2 patients (1 incorrectly). The presence of early mitral regurgitation predicted cardiovascular mortality at 1 year by univariate (relative risk, 12.2; 95% Cl, 3.5 to 42; P less than 0.0001) and multivariate (relative risk, 7.5; Cl, 2.0 to 28.6; P = 0.0008) analyses. Mitral regurgitation in early myocardial infarction is generally clinically "silent," is more common in anterior infarction, is associated with regional dysfunction but not early ventricular dilation or peak enzyme release, and is an important predictor of cardiovascular mortality.

The Marfan syndrome: Cardiovascular physical findings and diagnostic correlates

Correlations among cardiac symptoms and auscultatory and phonoechocardiographic findings in Marfan syndrome have not been completely defined. A total of 24 patients with Marfan syndrome (16 men and 8 women; mean age 28.2 ± 8.6 years) were studied. Mitral valve prolapse was noted in 22, of whom 19 had either nonejection systolic click or mitral regurgitation murmur. Mitral regurgitation was noted in 12 patients by Doppler imaging. Aortic root dilatation was noted in 20 patients and aortic regurgitation in six, five of whom had aortic regurgitation murmur (5 of 20 patients had undergone surgery). Proximal aortic dissection was noted in two. Dyspnea (n = 12) was associated with progressive mitral or aortic regurgitation in four, but in the others dyspnea could not be explained by valvular or ventricular abnormalities. Chest pain was related to pneumothorax in five and aortic dissection in two but was not associated with either in 15 patients. palpitations (n = 12) and lightheadedness (n = 6) were not associated with specific arrhythmias. In conclusion, mitral valve prolapse and aortic root dilatation were the most common cardiovascular abnormalities in Marfan syndrome. Mitral valve prolapse was frequently associated with typical auscultatory findings and symptoms including dyspnea, chest pain, palpitations, and lightheadedness, whereas aortic root dilatation could be clinically silent unless complicated by aortic regurgitation or aortic dissection.

Significance of a mitral regurgitation systolic murmur complicating a first acute myocardial infarction in the coronary care unit -- assessment by colour Doppler flow imaging

To determine the prevalence and significance of a systolic mitral murmur heard after a first acute myocardial infarction (MI), we studied 186 consecutive patients in the coronary care unit (CCU) during a one-year period. Fifteen patients had a murmur as a result of mitral regurgitation (MR) (prevalence 8%) documented by colour Doppler flow imaging. It was heard before the third day of hospitalization in 10 (67%) patients, and on the third day itself in the remainder. The severity of MR was graded semi-quantitatively: moderate in 12 (80%) patients, and mild, moderate to severe and severe in three respectively. The direction of the MR jet, determined by colour flow imaging, improved the information obtained by two-dimensional echocardiography (2D echo) that could only diagnose mitral leaflet abnormality in seven (47%) patients. In 10 of 15 (67%) patients, the 2D echo ejection fraction was greater than or equal to 40% and in eight (53%) the wall motion score obtained by analysing 11 left ventricular (LV) segments was less than or equal to 8. Two (13%) patients died in the CCU, four (27%) had LV failure, one angina and eight (53%) remained asymptomatic in the hospital. Of 171 patients without a systolic murmur, 22 (13%) had LV failure, 13 (8%) angina and 25 (15%) died during the in-hospital stay (P-NS for these complications between patients with and without MR murmur). During a follow-up of 12-24 months, one MR patient died, and seven (47%) remained asymptomatic. We conclude that the prevalence of MR systolic murmurs in acute MI patients is low.(ABSTRACT TRUNCATED AT 250 WORDS)

Kikuchi's Histiocytic Necrotizing Lymphadenitis: Report of a Case

Kikuchi's Histiocytic Necrotizing Lymphadenitis: Report of a Case