Late Systolic Murmur Research Articles

Blurred vision: Hitting the bull's eye

An 18-year-old female presented with progressive blurred vision in both eyes. On evaluation, her uncorrected visual acuity was 20/400 in both eyes. Slit lamp examination revealed bilateral supero-temporal dislocated lens splitting the pupillary axis with visible stretched zonules (Fig. 1). Intraocular pressure and posterior segment evaluation were normal. Systemic examination revealed a late systolic murmur at the apex.

A Rare Case of Ischaemic Stroke in A Young Man with Mitral Valve Prolapse

Mitral valve prolapse is a common valvular abnormality. It affects 2-3% of the general population. It often runs a benign course and the majority of patients are asymptomatic. Cardiac sources of thrombi account for about 20% of ischaemic strokes. There is lingering uncertainty regarding the causal link between mitral valve prolapse and ischaemic stroke. It has been suggested that changes on the surface of the valvular leaflets trigger platelet adherence and aggregation, leading to formation of platelet-fibrin thrombus which can embolize to the cerebral arteries, causing an ischaemic stroke. We herein report a case of a 25 year old young man who presented with sudden onset of left-sided weakness. Cardiac auscultation was notable for a late systolic murmur preceded by a midsystolic click at the apex. Transthoracic echocardiography showed an elongated and thickened anterior mitral valve leaflet which prolapsed into the left atrium during systole. Computed tomography scan of the brain revealed infarcts in the right frontal lobe and the right insular cortex. A diagnosis of myxomatous mitral valve prolapse complicated by ischaemic stroke was made and the patient was accordingly started on anticoagulant therapy with warfarin.

Cardio-vocal Syndrome as a Complication Patient with Severe Mitral Regurgitation and Moderate Aortic Regurgitation with Pulmonary Hypertension

ABSTRACT Hoarseness due to paralysis of vocal cord, as in Cardio-vocal syndrome, is caused by mechanical affection of left recurrent laryngeal nerve from enlarged cardiovascular structures. Mitral valve prolapse is rarely found to cause this syndrome. Case report presenting a 47 years old male visited the outpatient department with a clinical history of dyspnea and hoarseness since a year ago. Physical examination revealed late systolic murmur in apex and low-grade diastolic murmur in right second intercostal space. Echocardiography confirmed severe mitral regurgitation due to flail anterior mitral valve leaflet with severe left atrium dilatation (9.0 cm) and moderate aortic regurgitation due to mal-coaptation of aortic valves. Laryngoscopy revealed an immobile left vocal cord. He underwent successful double valve replacement after three months follow up the patient showed improvement of hoarseness. The incidence of Cardio-vocal syndrome in mitral valve disease varies from 0.6% to 5%. In cases diagnosed with thoracic disease, paralysis of the left vocal cord was reported 1.75 times more frequent than the right side. The aim of this case report is we have to aware that Cardio-vocal syndrome is a rare cause of vocal cord paralysis and should be considered as a differential diagnosis of hoarseness, particularly if the patient has a cardiac history. Comprehensive evaluation and prompt treatment may allow reversal of the damage to left recurrent laryngeal nerve. Permanent nerve damage can occur due to late diagnosis. Keywords : Cardio-vocal syndrome, Mitral regurgitation, Aortic RegurgitationCorrespondence : adityobasworo@gmail.com

Asymptomatic Coarctation of the Aorta in a Middle-Aged Man; The Significance of Physical Examination

Asymptomatic Coarctation of the Aorta in a Middle-Aged Man; The Significance of Physical Examination

ECG Challenge: March 17, 2015

HomeCirculationVol. 131, No. 11ECG Challenge: March 17, 2015 Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBECG Challenge: March 17, 2015 Originally published17 Mar 2015https://doi.org/10.1161/CIRCULATIONAHA.115.015990Circulation. 2015;131:1035A 58-year-old woman with a history of a previous myocardial infarction and mild mitral regurgitation presents to her cardiologist for a routine office visit. Her only medicines are aspirin and hydrochlorothiazide for mild hypertension. She is asymptomatic, and her physical examination is remarkable for a grade 3/6 late systolic murmur heard best at the apex. The result of the physical examination is normal except for an irregular pulse. An ECG was obtained.Download figureDownload PowerPointWhat is the diagnosis?To submit your diagnosis, go to http://circ.ahajournals.org/letters/submit/circulationaha;131/11/1035. The diagnosis will follow in the March 24 issue.Please go to the journal’s Facebook page for more ECG Challenges: http://goo.gl/cm4K7. Challenges are posted on Tuesdays and Responses on Wednesdays.FootnotesCorrespondence to Philip J. Podrid, MD, West Roxbury VA Hospital, Section of Cardiology, 1400 VFW Pkwy, West Roxbury, MA 02132. E-mail [email protected] Previous Back to top Next FiguresReferencesRelatedDetails March 17, 2015Vol 131, Issue 11 Advertisement Article InformationMetrics © 2015 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.115.015990 Originally publishedMarch 17, 2015 PDF download Advertisement SubjectsEchocardiography

Wavelet-based denoising method for real phonocardiography signal recorded by mobile devices in noisy environment

The main obstacle in development of intelligent autodiagnosis medical systems based on the analysis of phonocardiography (PCG) signals is noise. The noise can be caused by digestive and respiration sounds, movements or even signals from the surrounding environment and it is characterized by wide frequency and intensity spectrum. This spectrum overlaps the heart tones spectrum, which makes the problem of PCG signal filtrating complex. The most common method for filtering such signals are wavelet denoising algorithms. In previous studies, in order to determine the optimum wavelet denoising parameters the disturbances were simulated by Gaussian white noise. However, this paper shows that this noise has a variable character. Therefore, the purpose of this paper is adaptation of a wavelet denoising algorithm for the filtration of real PCG signal disturbances from signals recorded by a mobile devices in a noisy environment. The best results were obtained for Coif 5 wavelet at the 10th decomposition level with the use of a minimaxi threshold selection algorithm and mln rescaling function. The performance of the algorithm was tested on four pathological heart sounds: early systolic murmur, ejection click, late systolic murmur and pansystolic murmur.

Bilateral giant coronary aneurysms in a 40-year-old male with Noonan syndrome caused by a KRAS germline mutation

We report a case of a 40-year-old man who was admitted to our hospital for the evaluation and treatment of chest discomfort on exertion. He had previously been followed for post-natal growth deficiency, strabismus, mental retardation, epilepsy, and moderate mitral regurgitation. On admission, he was 142 cm in height and 42 kg in weight. Physical examination revealed orbital hypertelorism, ptosis, a webbed neck, and low-set ears with no jugular vein dilatation or peripheral edema. Cardiac auscultation showed a 3/6 late systolic murmur and S4. ECG showed normal sinus rhythm, poor R wave progression in the precordial leads, and an incomplete right bundle brunch block. Chest X-ray showed pulmonary congestion and marked cardiomegaly, with a cardio-thoracic ratio of 71%.

Design Electronic Stethoscope for Cardiac Auscultation analyzed using Wavelet Decomposition

Stethoscope become standard equipment used medical personnel to perform initial checks on patients. Stethoscope in general has a function for auscultation, which is listening to the sounds that occur in the body. The sound produced by the biological activity of the body's organs, like the heart, lungs and digestive system. The heart is one organ that plays a role in the circulatory system. Contraction of the heart that can cause pulsation felt in the arteries in some places. Instrument used for the detection of clinically sound heart is an acoustic stethoscope. Acoustic stethoscope has a weakness, depending on the hearing of each physician. Diagnosis of each physician may vary. Sensitivity of the ear of each doctor is different. Noise signals generated in the electronic stethoscope will be analyzed using Wavelet. In this research, recognition of heart sounds using a stethoscope sound signal based on wavelet decomposition. Heart sound signal is decomposed up to level 8 using Daubechies 3 wavelet (db3). Energy of each subband is calculated spectogram. Analysis of cardiac auscultation signals with wavelet daubachies, system can calculate the value of heartrate with 78% for heart sound pattern of early and late systolic murmur, 63% Diastolic heart sound patterns Rumble and 85% for normal heart sound patterns.

Auscultatory manifestations of mitral valve prolapse in children with connective tissue dysplasia

Aim. To study the features of auscultatory symptoms in children with mitral valve prolapse secondary to connective tissue dysplasia. Methods. Auscultation and phonocardiography was performed in 545 children and adolescents with mitral valve prolapse, including a prolapse, which is a variant of the asthenic constitution - 140, with a prolapse with undifferentiated connective tissue dysplasia - 340, with mitral valve prolapse with differentiated connective tissue dysplasia - 65 children (patients with Marfan syndrome and Ehlers-Danlos syndrome). The control group consisted of 200 children and adolescents of similar age. Results. In children with an asthenic constitution and mitral valve prolapse in most cases (90.7%) established were isolated clicks, and only iin a small percentage of cases the clicks combined with the late systolic murmur. Complaints of these children did not differ significantly in the frequency from the control values. Compared with the control group up to 6 times more frequently found was the symptom of chronic psychoemotional stress. Chronic psychoemotional stress was also observed more frequently in adolescents with mitral valve prolapse in the background of undifferentiated and differentiated connective tissue dysplasia. Children with asthenic constitution the frequency of cardiac pain did not differ from the control values. A significant increase in the frequency of cardialgia was reported in children and adolescents with undifferentiated and differentiated connective tissue dysplasia. Cardiac pain was described as stabbing, pressing, aching, and was felt in the left side of the chest without irradiation. In most children the pain continued for 5-20 min, were usually enduced by physical exertion and emotional stress, often accompanied by autonomic disturbances, which resolved spontaneously or after administration of the tincture of valerian or valokordin. The absence of ischemic changes in the myocardium according to the comprehensive investigation can be regarded as a manifestation of cardialgia as a sympathalgia related to psychoemotional features of children with mitral valve prolapse («cardiac pain is inseparable from the personality»). The auscultatory pattern suring mitral valve prolapse in the background of undifferentiated and differentiated connective tissue dysplasia was very similar. Conclusion. According to the phonocardiography and auscultatory data we can conclude that there is a certain parallelism of the severity of valve leaflet prolapse and of the sound phenomena: in isolated clicks the leaflet prolapse degree is usually minor, however in cases of isolated late systolic and holosystolic murmurs - the prolapse degree is significant.

Case of the Month #174: Papillary Fibroelastoma of the Aortic Valve

A 53-year-old woman with a history of mitral valve prolapse and hyperthyroidism presented to the emergency department with nonradiating chest pain (‘‘pins and needles in the heart’’). She also had worsening shortness of breath on exertion and weakness and weight loss over a 3-month period. On physical examination, her heart rate was 110 beats per minute and respiratory rate was 18 per minute. Cardiac auscultation revealed a late systolic murmur over the mitral area that radiated to the axilla. Pulmonary examination was normal. Transthoracic echocardiography showed a mitral valve prolapse, withmild regurgitation. It also revealed a 9 10-mm mass on the left coronary cusp of the aortic valve. Transesophageal echocardiography (Figure 1) showed the mobile pediculated mass attached to the base of the aortic surface of the left coronary cusp of the aortic valve as well as thickening of the cusp. Anterior leaflet prolapse of the mitral valve with moderate regurgitation also was demonstrated. Cardiac magnetic resonance (MR) imaging quantified the prolapse of the mitral valve as moderate. The aortic valve lesion, however, was poorly visualized. An electrocardiographic (ECG) gated contrast-enhanced cardiac computed tomography (CT), performed for preoperative assessment of the coronary arteries, allowed visualization of a 8-mm aortic valvular lesion, on the aortic surface of the valve (Figure 2). Surgery revealed the lesion of the aortic valve located on the

Orthostatic intolerance and coronary reserve: a matter of a certain gravity

A 74-year-old woman came to our attention complaining of the recent onset of shortness of breath during light physical activity. She reported orthostatic light-headedness, occasional dizziness, and pre-syncope symptoms for a duration of the prior year. The past history included mitral valve prolapse with mild regurgitation, dyslipidemia, and paroxysmal atrial fibrillation. At presentation, the current medications included propafenone, aminosalicylic acid, and simvastatin. A 24-h-ECG demonstrated the presence of polymorphic ventricular premature beats and asymptomatic ST-segment depression. The treadmill exercise test showed limited exercise tolerance, and a significant downward sloping ST-segment depression in leads V4–V6 at the beginning of step 2 of the Bruce protocol. An exercise myocardial perfusion scan was consistent with a reduced coronary reserve of the anterior wall. Upon admission, lying and up-right arterial pressures were 130/80 and 90/50 mmHg, respectively, while a physical examination documented a systolic click and a late systolic murmur. After medications were suspended, a new treadmill exercise test (Fig. 1, left panel) demonstrated orthostatic hypotension [1] with tachycardia upon standing, and a further decline of arterial pressure and heart rate increase during the Bruce stage 1. Exercise was interrupted due to pre-syncope symptoms after 204600 when 88% of the predicted maximal heart rate had been reached, and ST depression (-1.0 mm, V5–V6) observed. Considering the patient’s characteristics, the estimated pre-test probability of a significant coronary stenosis was 20–50% [2, 3]. The positive likelihood ratio of exercise stress test and myocardial perfusion scan for a significant coronary artery disease was about 10[4]. Thus, the patient’s post-test probability of a significant coronary stenosis was in the 70–90% range. A coronary angiography was thus performed, but ruled out a stenosis of the major coronary vessels. In the absence of stenosis, a reduction of coronary reserve may be secondary to functional mechanisms [5], including the originally misdiagnosed orthostatic hypotension. We thus hypothesized a critical decline in coronary blood flow during upright physical activity due to an exercise-induced significant decrease in arterial pressure on a pre-existing orthostatic hypotension background. To test our hypothesis, an exercise bicycle test was performed in the lying posture, a position unlikely to affect arterial pressure. Exercise was interrupted at 703500 because of physical exhaustion (Fig. 1, right panel). Neither a significant reduction in arterial pressure nor ST-segment changes was observed along the exercise-induced heart rate increase. The maximum heart rate systolic pressure product [6], a broad index of cardiovascular function, increased more when exercise was performed in a lying position than during up-right posture, compared to baseline, although the increase in heart rate was lower in the supine than in the standing position (Fig. 1). G. Costantino Medicina Interna II, Ospedale Sacco, Milan, Italy

Mitral Valve Prolapse With a Late-Systolic Regurgitant Murmur May Be Associated With Significant Hemodynamic Consequences

The late-systolic murmur of mitral regurgitation (MR) in degenerative mitral valve disease is widely believed to represent regurgitation of a degree that is not associated with hemodynamic significance. However, the extent of left ventricular (LV) remodeling associated with the late-systolic murmur has not been systematically assessed. Accordingly, we studied 82 patients sent for evaluation of at least moderate isolated MR by echocardiography/Doppler examination. All patients had a physical examination and cardiac magnetic resonance imaging to measure LV volumes by summation of serial short-axis slices. Forty-five patients had a pan-systolic murmur and 37 had a late-systolic murmur on auscultation that was verified by timing of onset of regurgitant turbulence by cine magnetic resonance imaging. Systolic blood pressures (124 ± 3 versus 124 ± 3mm Hg) and LV ejection fraction (61 ± 1% versus 61 ± 1%) did not differ significantly between pan-systolic and late-systolic murmur groups. Although LV end-diastolic volume index was greater in the pan-systolic versus late-systolic murmur (108 ± 4 versus 95 ± 4mL/m2, P=0.007), both groups were significantly greater than normals (68 ± 2mL/m2, P < 0.0001). However, LV end-systolic volume index (42 ± 2 versus 38 ± 2mL/m2) and LV end-systolic dimension (38 ± 1 versus 37 ± 1mm), critical markers of adverse LV remodeling in isolated MR, did not differ significantly between pan-systolic and late-systolic murmur groups. In conclusion, the late systolic isolated MR murmur may be associated with significant adverse LV remodeling, and should not be considered evidence of hemodynamically unimportant MR.

Isolated cleft of the posterior mitral valve leaflet

Fig. 1. A: Late-systolic still-frame of a transthoracic short axis view depicts the cleft (⁎) of the mildly thickened posterior mitral leaflet. AML denotes anterior mitral leaflet. B: Colour Doppler showing a moderate mitral regurgitation. A 64-year-old lady was referred for evaluation of a recently detected heart murmur. The patient was completely asymptomatic and an avid tennis player. Auscultation revealed a loud midto late systolic click followed by a grade III midto late systolic regurgitant murmur. Transthoracic echocardiography showed an isolated cleft of the mildly thickened posterior mitral valve leaflet with a moderate late systolic mitral regurgitation (Fig. 1). The anterior mitral valve leaflet and the subvalvular apparatus were normal, especially the insertion of the papillary muscles. No other cardiac anomalies were present. Isolated cleft posterior mitral valve leaflet is a very rare congenital malformation that is usually diagnosed in early childhood. The cleft is more commonly found in the anterior leaflet and in association with other cardiac anomalies such as atrioventricular septal defects and anomalies of the papillary muscles [1,2]. A retrospective analysis of more than 13,000 children revealed only ten isolated cleft mitral valve leaflets with none of them affecting the posterior leaflet [3]. Cleft mitral valve leaflet may result in severe mitral regurgitation and the need for surgical repair [4]. Our patient was diagnosed with the malformation at age sixty-four, had only moderate mitral regurgitation and remained asymptomatic.

Reversal of Acute Pulmonary Oedema with Beta-blockers in Hypertrophic Cardiomyopathy

A 41-year old male was admitted with dyspnoea in 1990. His ECG demonstrated sinus rhythm, voltage-criteria for left ventricular hypertrophy and Q waves in the lateral leads. Transthoracic echocardiography demonstrated asymmetrical septal hypertrophy (17 mm), partial systolic anterior movement of the anterior mitral valve leaflet, a dynamic sub-aortic gradient of 30 mmHg and the presence of diastolic dysfunction as demonstrated by a reversal of the E:A ratio. The diastolic dysfunction was thought to be responsible for the patient’s presenting symptoms. Hypertrophic cardiomyopathy (HCM) was diagnosed but the patient declined any medical treatment or follow-up. He presented in June 2000 with a right hemiparesis. The ECG on admission showed atrial fibrillation with a ventricular rate of 110 beats per minute (bpm). Computerized tomography of the brain did not reveal evidence of a haemorrhagic bleed and treatment was commenced with intravenous heparin and an oral anticoagulant. An echocardiogram on day 5 demonstrated no changes from his previous study. In the absence of a severe outflow tract gradient, he was commenced on verapamil 120 mg twice daily, for ventricular rate control and treatment of diastolic dysfunction. On day 18, the patient became acutely dyspnoeic. Examination revealed a heart rate of 65 bpm, blood pressure of 120/70 mmHg, a late systolic murmur loudest at the left sternal edge and crackles throughout the lung fields. A chest radiograph confirmed pulmonary oedema and treatment with intravenous diuretics and oxygen therapy was immediately initiated. The patient was unresponsive to therapy and so an emergency echocardiogram was performed. This revealed normal systolic function of the left ventricle, a maximum dynamic gradient of 150 mmHg in the left ventricular outflow tract and mild mitral regurgitation (Fig. 1). An intravenous bolus of esmolol was administered and within 10 min there was rapid improvement in the patient’s symptoms. Real-time echocardiography demonstrated a dramatic reduction in the outflow tract gradient to 16 mmHg (Fig. 2). An esmolol infusion was continued for a further 8 h and then replaced with oral beta-blocker therapy. The remainder of the patient’s stay was uneventful and he was discharged on oral

Mechanism of mitral regurgitation in inferior wall acute myocardial infarction

I 1963, Burch et al 1,2 reasoned that infarction of a papillary muscle causing failure to contract during ventricular ejection would result in mitral valve prolapse during the latter half of systole. This concept was developed to explain the timing of the murmur observed in ischemic mitral regurgitation (MR), which is frequently midto late systolic. However, experimentally induced isolated papillary muscle damage, ischemia, and infarction have repeatedly failed to produce MR. Also, MR caused by prolapse is not observed clinically in acute myocardial infarction or ischemia. Instead, similar to functional MR in idiopathic dilated cardiomyopathy, the mitral leaflets have been found to be apically displaced, showing incomplete leaflet closure. This has been attributed to dyskinesia or distortion of the region of the left ventricle from which the papillary muscles arise, displacing the papillary muscles and thus restricting leaflet closure. Nevertheless, the theory of papillary muscle dysfunction causing prolapse has survived even into recent editions of cardiology textbooks. One of the reasons may be the lack of an alternative explanation for the late systolic murmur in ischemic MR. Such an explanation may be found in the pattern of phasic regurgitant orifice area variation during systole, which reflects the underlying mechanism of MR. In idiopathic dilated cardiomyopathy, echocardiographic recordings of the proximal flow convergence region during MR have demonstrated a distinct biphasic pattern of flow and orifice area variation: a decrease during left ventricular contraction, an increase during ventricular relaxation. We hypothesized that the pattern of regurgitant orifice area variation in ischemic MR due to inferoposterior wall motion abnormalities will be similar, because the observed geometric substrate of regurgitation—apical tenting of the mitral valve—suggests a similar mechanism. In particular, we sought to demonstrate that the phenomenon of late systolic murmur can be explained by a late systolic increase in regurgitant orifice area and flow, a variant of the biphasic pattern of functional MR, and that it is related to mitral leaflet tethering and not mitral valve prolapse.

Toward an Understanding of the Cause of Mitral Valve Prolapse

Toward an Understanding of the Cause of Mitral Valve Prolapse

Auscultation in Mild Mitral Regurgitation in Dogs: Observer Variation, Effects of Physical Maneuvers, and Agreement with Color Doppler Echocardiography and Phonocardiography

Observer variation in diagnosing mild mitral regurgitation in dogs by cardiac auscultation was assessed by having 6 veterinarians with different levels of experience examine 57 Cavalier King Charles Spaniels. Comparisons with color Doppler echocardiography and phonocardiography were made, and the effects of 2 physical maneuvers on the auscultatory findings were evaluated. Using mildly diseased dogs, interobserver agreement in diagnosing the presence or absence of left-sided murmurs ranged from 63% to 88%. The agreement with phonocardiography (range, 53-91%) increased with the amount of observer experience. The 2 most experienced observers could discern soft ejection murmurs from regurgitant murmurs and were able to diagnose 89% of the dogs with regurgitant jets larger than 30% of the left atrial area. In general, less experienced observers diagnosed most jets larger than 50%. In many dogs with small jets, no murmur was found by auscultation and phonocardiography. The audibility of mild regurgitation was significantly reduced in dogs that were difficult to auscultate. Early systolic murmurs were typical of mild regurgitation, whereas holosystolic murmurs typified severe regurgitation. In a few dogs, late systolic murmurs alternated with holosystolic murmurs. Systolic clicks were found phonocardiographically in 18 dogs with mild to moderate regurgitation, but the audibility apparently was low. In many mildly affected dogs, physical maneuvers increased murmur intensity. Thus, some form of dynamic auscultation might facilitate the diagnosis of mild regurgitation. Auscultatory findings in mild regurgitation appear to depend on observer experience, circulatory status, and how difficult the dog is to auscultate.

Mitral Valve Prolapse in Active Patients.

In brief In most people, mitral valve prolapse, which affects women more than men, is a benign condition with few or no symptoms. But in some patients it poses a significant problem. Potential sequelae include endocarditis, serious arrhythmia, and sudden death. Although a midsystolic click followed by a late systolic murmur is characteristic, definitive diagnosis requires echocardiography. Treatment ranges from education and reassurance in those who have mild disease to valve replacement in severe cases. Most athletes who have mitral valve prolapse can safely participate in all activities. Those with evidence of significant valvular disease, serious arrhythmia, or a family history of sudden death due to mitral valve prolapse, however, should participate only in low-intensity competitive sports.

Mitral Valve Prolapse in Active Patients

In most people, mitral valve prolapse, which affects women more than men, is a benign condition with few or no symptoms. But in some patients it poses a significant problem. Potential sequelae include endocarditis, serious arrhythmia, and sudden death. Although a midsystolic click followed by a late systolic murmur is characteristic, definitive diagnosis requires echocardiography. Treatment ranges from education and reassurance in those who have mild disease to valve replacement in severe cases. Most athletes who have mitral valve prolapse can safely participate in all activities. Those with evidence of significant valvular disease, serious arrhythmia, or a family history of sudden death due to mitral valve prolapse, however, should participate only in low-intensity competitive sports.

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.