Opening Snap Research Articles

Where Has the Awe in Medicine Gone? Part I

Do you remember when you started medical school and received your first white coat? That symbol made us feel like real doctors, and all the energy and effort that was spent to reach that ceremony was worth it. How about the first time you were in the labor and delivery room and participated in the birth of a baby? Or how about the first time you conducted a history, performed a physical exam, wrote findings for the proctor, and functioned like a real doctor? Or how about when you were making rounds with the chief resident, and they told you where to put your stethoscope so you might hear the opening snap of mitral stenosis ... and you really did hear it? These were those special moments that made you feel exhilarated and provided you with a sense of awe. This article defines awe and its benefits to healthcare providers.

Abstract 11386: Double Whammy Complicating Management of Pulmonary Hypertension

Introduction: When presented with challenging cardiac cases, in addition to obvious diagnoses, it is critical to maintain high level of suspicion about other subtle conditions. We describe one such case of pulmonary arterial hypertension (PAH) from severe mitral stenosis (MS) and another less obvious congenital cardiac condition that significantly impacted the clinical course. Case: 32-year-old immigrant male with known heart murmur presented with palpitations due to atrial fibrillation. His resting oxygen saturation was 95% in all extremities and he had no clubbing. He had pectus carinatum and scoliosis, prominent right ventricular lift, normal S1, loud S2, opening snap, rumbling diastolic murmur at the apex, and an ejection systolic murmur at the left upper sternal border. Echocardiogram revealed normal biventricular size and function, severely enlarged left atrium, rheumatic severe MS, moderate mitral regurgitation, a restrictive ventricular septal defect (VSD), and elevated right ventricular systolic pressure. Cardiac catheterization demonstrated mixed pre- and post-capillary PAH with mean pulmonary artery pressure of 80 mmHg, wedge pressure 30 mm Hg and pulmonary vascular resistance of 3.0 woods unit which was underestimated. Since pre-capillary component of the PAH could not be entirely explained by the small VSD, a congenital cardiac CT was performed revealing moderate sized patent ductus arteriosus (PDA). Further management decisions were complicated since MS was not amenable to percutaneous intervention and surgical risks were high given severe pre-capillary PAH- management of which with pulmonary vasodilators was itself high risk in the setting of severe MS and high wedge pressures. After optimal medical management, a multidisciplinary team carefully considered the risks and benefits of multiple interventions. Ultimately, the patient underwent surgical mitral valve replacement, fenestrated patch closure of the PDA, and then initiation of pulmonary vasodilators. The patient continues to do well on oral pulmonary vasodilator therapy 6 months after surgery. Conclusion: We describe an astute critical thought process of a multidisciplinary team utilized to manage a challenging case of mixed PAH from severe rheumatic MS and PDA.

71-Year-Old Man With a New Heart Murmur

71-Year-Old Man With a New Heart Murmur

LOOKING DEEPER INTO MITRAL REGURGITATION

A 50 years old male patient previously treated for pulmonary Kochs presented with shortness of breath (functional class II). A non-ejection click and pan-systolic murmur radiating to axilla was heard at apex. Transthoracic echocardiography revealed thickened and markedly prolapsing both leaflets of mitral valve with mild to moderate regurgitation. A clear space was noted between the termination of LV myocardium and atrio-mitral junction (7.7mm) indicating Mitro-annular disjunction (MAD). 24 hours Holter monitoring showed 160 isolated premature ventricular contractions, maximum 20 in one hour. No other arrhythmia was recorded. Beta blocker and an ACE inhibitor were initiated with advice for follow-up as presently no intervention was needed.

Additional Heart Sounds–Part 2 (Clicks, Opening Snap and More)

Abstract Systolic clicks are high-pitched sharp sounds. They are classified as ejection and nonejection clicks. Ejections clicks commonly occur at the aortic and pulmonary valve, while nonejection clicks occur at the mitral and tricuspid valve. Opening snap is an additional sound heard in the diastole. It is described as an early diastolic, high-pitched sound, which is associated with opening of the mitral and/or tricuspid valve. Pericardial knock is a high-pitched early diastolic sound, which is characteristic of constrictive pericarditis. The opening and closing of prosthetic valves produce sounds which may vary in intensity and timing according to the type and design of the valve, patient’s rhythm, and hemodynamic status.

Pathological discrimination of the phonocardiogram signal using the bispectral technique.

Phonocardiography is a dynamic non-invasive and relatively low-cost technique used to monitor the state of the mechanical activity of the heart. The recordings generated by such a technique is called phonocardiogram (PCG) signals. When shown visually, PCG signals can provide more insights of heart sounds for medical doctors. Thus, several approaches have been proposed to analyse these sounds through PCG recordings. However, due to the complexity and the high nonlinear nature of these recordings, a computer-assisted technique based on higher-order statistics HOS is shown to be, among these techniques, an important tool in PCG signal processing. The third-order spectra technique is one of these techniques; known as bispectrum, it can provide significant information to support physicians with an accurate and objective interpretation of heart condition. This technique is implemented and discussed in this paper. The implemented technique is used for the analysis of heart severity on nine different PCG recordings. These are normal, innocent murmur, coarctation of the aorta, ejection click, atrial gallop, opening snap, aortic stenosis, drum rumble, and aortic regurgitation. A unique bispectrum representation is generated for each type of heart sounds signal. Then, based on the bispectrum analysis, fifteen higher-order spectra HOS features such as the bispectral amplitude, the entropies, the moments, and the weighted center are extracted from each PCG record. The obtained HOS-features showed a well-correlated evolution with the increasing importance of heart severity leading therefore to a high potential in discriminating pathological PCG signals. One should know that, generally, classification of pathological PCG signals refers to the distinction between the presence of a pathology from its absence (binary response) while the discrimination considered in this paper provides an analogue response (value) which can vary from one pathology to another in an increasing or decreasing way.

THE MAN WITH THREE ATRIUMS: COR TRIATRIATUM SINISTER

SESSION TITLE: Medical Student/Resident Genetic and Developmental Disorders Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Cor triatriatum sinister (CTS) is a rare congenital cardiac condition characterized by the division of the left atrium by an abnormal fibromuscular membrane potentially causing obstruction of blood flow within the left atrium. The condition is found in less than 0.1% of patients diagnosed with cardiomyopathies and typically diagnosed in childhood. We describe a case of an incidentally diagnosed CTS in an adult. CASE PRESENTATION: A 45-year old male with a past medical history of supraventricular tachycardia and coronary artery disease status post percutaneous stenting was admitted to the hospital for evaluation of shortness of breath, productive cough, fever and chills. On chest x-ray, there was evidence of a left lower lobe pulmonary infiltrate and he was treated for community acquired pneumonia with ceftriaxone and azithromycin. His hospital course was complicated by hypoxemic respiratory failure. Echocardiography was performed, due to persistent tachycardia and shortness of breath and he was found to have CTS (Figure 1). On further questioning he declined a history of dyspnea on exertion, orthopnea or other respiratory complaints since childhood. He was discharged home after resolution of acute community-acquired pneumonia. DISCUSSION: There are three theories on the embryology of CTS; malincorporation, malseptation and entrapment. Among these, malincorporation of the common pulmonary vein into the left atrium creating two chambers separated by a narrowing chamber, is the most accepted theory. Up to 80% of cases are associated with other congenital abnormalities and presentation varies from asymptomatic patients to septic shock with pulmonary edema and respiratory failure. In adults, asymptomatic patients likely have a large foramen (fenestrations) with no intra-atrial pressure gradient unlike symptomatic patients who have no means for compensation and develop elevated left atrial pressure and subsequent pulmonary congestion. On physical exam, no pathognomonic findings are seen, and the absence of an opening snap or loud S1 differentiates the murmur of CTS from mitral stenosis. Echocardiography is a simple, non-invasive tool that can delineate the morphology and diagnose CTS as well as assess severity, describing severe obstruction when the doppler velocity gradient is greater than 2 m/s. Further studies are not needed, but cardiac catheterization, and cardiac magnetic resonance imaging can be useful for diagnosis and management. Management is based on symptoms and ranges from no treatment, to preload reducing agents, to surgical intervention. CONCLUSIONS: Establishing the diagnosis is critical as untreated, hemodynamically-significant CTS can lead to arrhythmias, pulmonary hypertension and right-sided heart failure that can be prevented with favorable outcomes after surgical correction. We present this case due to its rarity and asymptomatic nature in an adult patient. Reference #1: Nassar PN, Hamdan RH. Cor triatriatum sinistrum: classification and imaging modalities. The European journal of cardiovascular medicine. 2011;1(3):84. Reference #2: Ather B, Siddiqui WJ. Cor Triatriatum. In: StatPearls [Internet]. StatPearls Publishing; 2019. Reference #3: Chen Q, Guhathakurta S, Vadalapali G, Nalladaru Z, Easthope RN, Sharma AK. Cor triatriatum in adults: three new cases and a brief review. Tex Heart Inst J. 1999;26(3):206-210. DISCLOSURES: No relevant relationships by Israel Acosta Sanchez, source=Web Response No relevant relationships by Floyd Burke, source=Web Response No relevant relationships by Somshukla Ghosh, source=Web Response No relevant relationships by Hiren Patel, source=Web Response No relevant relationships by Irene Riestra Guiance, source=Web Response

Second Heart Sound

AbstractThe auscultation of second heart sound reveals presence of the disease and its pathophysiology, conduction defects, ventricular function, and hemodynamics around the aortic and pulmonary valves. To understand the splitting of the second heart sound, it is useful to understand the concepts of hangout interval and ejection time. Differential diagnosis of S2 split include opening snap, third heart sound, and pericardial knock. Variations of second heart sound may involve intensity or variations of split. Variations of split can be single heart sound, wide split, wide fixed split, or paradoxical splitting.Interpretation of second heart sound in congenital heart disease provides information about the presence and position of semilunar valves.

HEART MURMURS DETECTION AND CHARACTERIZATION USING WAVELET ANALYSIS WITH RENYI ENTROPY

Phonocardiogram signals (PCGs) represent a nonstationary signal due to their complicated production. Also, during the registration they may be added with different noise and pathological murmurs. Indeed, in real situation, the heart sound signal (HSs) may present some abnormal murmur characterizing a variety of heart diseases. This work deals with the segmentation of pathological PCGs based on the Discrete Wavelet Transform (DWT) which permits signal decomposition in different frequency bands. After the decomposition step, we estimate the Renyi Entropy (RE) of the detail coefficients. Then, we apply a threshold allowing detecting the murmur of the PCGs. After the detection, we characterize the results in time–frequency domain in order to extract some features such as frequency band, peak frequency and time duration of the abnormal murmur. The validation of the method is evaluated and proved using some pathological PCGs such as: Early Aortic Stenosis (EAS), Late Aortic Stenosis (LAS), Mitral Regurgitation (MR), Aortic Regurgitation (AR), Opening Snap (OS) and Pulmonary Stenosis (PS). The method presents good results in terms of the detection and the characterization of the main components and the abnormal murmurs associated with some valves disease.

Benfluorex-induced mitral stenosis: A misknown etiology

A 60-year-old Caucasian overweight female patient with history of three uneventful pregnancies and benfluorex intake 150 mg t.i.d. for eight years who developed progressive dyspnea over the past two years. No history of rheumatic fever was found. Cardiac auscultation revealed holosystolic murmur, opening snap and prolonged diastolic murmur. Chest X-ray revealed normal heart size, venous congestion and right pleural effusion (proteins 25 g/l). Echocardiography examination found normal ejection fraction, enlarged left atrial size, mild aortic regurgitation and mild-to-moderate mitral regurgitation with thickened and shortened leaflet and subvalvular apparatus, bicommissural fusion resulting in significant mitral stenosis (mean and maximal gradients were 16 and 28 mm Hg respectively) (Fig. 1 A,B, movie). Systolic transtricuspid gradient was 36 mm Hg. The patient underwent surgical valve replacement with a mechanical bileaflet valve. Per-operative findings were a funnel-shaped mitral apparatus, localized calcification on A3 and leaflet thickening with bicommissural fusion. The subvalvular apparatus was thickened and shortened with interchordal fusion (Fig. 1 C). Pathology examination demonstrated drug-induced valvular disease by showing non-inflammatory endocardial fibrosis that predominates on ventricular side of the valvular apparatus (Fig. 1 D). Due to vitamin K antagonist mediated excessive bleeding the patient died four years later.

Very early complication of rheumatic heart disease (valvuloplasty for severe mitral valve stenosis for 6 year old male patient)

Rheumatic heart disease continues to contribute greatly to the burden of cardiovascular disease in Yemen, It’s usual to see a lot of advance RHD cases in adult in Yemen but in pediatric it is rare to see such advance case specially under the age of eight. Case report A.M, a 6 year old Yemeni male child was seen in September 2012 with history of recurrent breathlessness which started about 4 years earlier. His symptoms worsened in the previous three weeks when he became breathless at rest, had paroxysmal nocturnal dyspnea, huge abdominal distention, bilateral leg swelling and cough productive of whitish sputum. Past history was not significant for recurrent sore throat but he was diagnosed to have RHD at age of 3 year old without any farther follow up and irregular using to long acting penicillin. He was the second child in his family; both parents are in a very low income group. There was no family history of the disease in any of his siblings. Examination revealed that the child looked marasmic, pale, was chronically ill, and had a tinge of jaundice with bilateral pitting pedal edema. A cardiovascular system examination revealed a pulse rate of 101 per minute, regular and small volume, blood pressure of 90/60 m mmHg, elevated jugular venous pressure, displaced apex beat which was located at 5th intercostal space anterior axillary line, loud first and second heart sounds opening snap and mid diastolic rumbling murmur with systolic murmur at left parasternal border. The respiratory rate was 26 cycles per minute and bilateral crepitations. Other examination findings were visible dilated abdominal vein, a tender, pulsatile hepatomegaly of 3 cm below the right coastal margin and massive ascites. An echocardiography showed densely thickened mitral valves with severe commissural fusion leading to doming of the mitral valve in diastole, markedly dilated left atrium, normal left ventricular eject ion fraction, markedly dilated right atrium and right ventricle. Colour flow showed severe tricuspid regurgitation and severe pulmonary hypertension. The calculated mitral valve area is 0.6 cm square and pressure gradient max/mean (14/6 mmHg) respectively. ECG sinus rhythm normal axis and dilated LA with RBBB Complete blood count showed low HB 9 mg/dl with normal a white cell count. The chest X-ray revealed cardiomegaly with a double cardiac shadow positive mitralization sign. He was placed on diuretics (furosemide and low-dose spironolactone) Angiotensin Converting Enzyme inhibitor (Lisinopril), intranasal oxygen, intravenous heparin and antibiotics. And was prepared for percutaneous mitral valvuloplasty On the third day of admission, The PMVP was done with good out come the mitral valve area increase from 0.6 to 1.8 cm 2 and decrease in the pressure gradient to 6/4 mmHg and the pulmonary hypertension to mild. After that patient condition get better with improving to the dyspnea, the child become more active start to eat and play more frequent than before with decrease to the abdominal distension and the patient discharge to home in good condition and advice to follow up the hospital after six month. Discussion Rheumatic heart disease, no doubt remains a disease with great morbidity and mortality in most low and middle income countries specially in Yemen despite been having almost eradicated in high income countries, it affects the young population of our community whom presented late most of the time with complication due to the shortage of the medical service in the most of the regain of Yemen specially the remote areas. The case being presented typifies the cost of late presentation in patients with rheumatic heart disease. its usual in our country to see such cases in late stage and complicated but it’s rare to see a 6 year old child presented with severe mitral stenosis and he needed PMVB even it is successful procedure that saved his live but all that could be prevented from happening in the first place by a simple preventive program which we do not have in our country.

Cor triatrium presenting as mitral stenosis and severe anemia

Cor triatrium presenting as mitral stenosis and severe anemia

Polypoid atrial myxoma

Myxomas are by far the most common tumours of the heart. A 75-year-old man with no notable medical history presented with a 2-month progressive weight loss and dyspnoea on exertion. Physical examination revealed an opening snap and a diastolic decrescendo murmur at the apex. Transthoracic echocardiography showed a large, 85 × 30 mm, mobile, polypoid mass arising from the atrial fossa ovalis and protruding into the left ventricle during diastole. Irregular shape, multilobated surface and soft-tissue echogenicity were consistent with emboligenic myxoma. Surgical inspection confirmed a reddish gelatinous myxoma with villous, friable, thrombus-like surface prone to embolize. The mass was successfully removed and the histologic report confirmed the diagnosis.At 3-year follow-up, the patient is asymptomatic and no further mass has been detected. The case confirms that echocardiography remains a primary tool for the assessment of cardiac masses, providing morphological clues to define the potential risk of complications such as valve obstruction and systemic embolization.

Obstructive giant cardiac tumour in a patient with chest pain and acute respiratory insufficiency

A 77-year-old woman presented with dyspnoea and respiratory-related thoracic pain, which was accompanied by dizziness and fatigue but no syncopal attacks. Auscultation of the heart disclosed an opening snap with mid-diastolic murmur. Laboratory assessment revealed no abnormalities but an elevated D-dimer level (1.49 mg/l). Electrocardiography was normal. The chest radiograph showed an enlarged heart without other abnormalities. Computed tomography (CT) scan for a suspected diagnosis of pulmonary embolism was performed. The CT scan did not reveal pulmonary embolism, but a large cardiac tumour in the left atrium.

A pinball game in the left atrium

In January, 2011, a 64-year-old woman presented to us with atwo-week history of fatigue, dizziness, dyspnea on exertion, andpain in the fourth and fifth toes of her left foot. One year before, shewas diagnosed with atrial fibrillation and moderate rheumaticmitral valve stenosis. On that occasion, a transesophagealechocardiography showed a mural thrombus stuck to the posteriorwall of the left atrium, whose diameters were 3×5 cm. Therefore,anticoagulation with warfarinwas begun. A follow-up echocardiogra-phy documented the persistence of the thrombus five months beforepresentation, despite regular anticoagulation. Her thrombophiliawork-up was negative. On physical examination there was inceptivegangreneof the fingertipof the fourthtoe of her left foot. She had pal-pable bilateral femoral, popliteal, and posterior tibial pulse and a re-duced dorsalis pedis pulse. Heart auscultation was notable for aloud first heart sound, an opening snap, and a mid-diastolic murmur.The murmur changed in intensity randomly, independently by posi-tion of the patient or inspiration. Chest radiographyrevealeda dilatedleft atrium, pulmonary venous congestion, and enlarged pulmonaryartery.ECG showed atrialfibrillation. Transthoracic echocardiographyrevealed a large highly mobile mass in the left atrium. Transoesopha-geal echocardiography showed a round floating mass in the left atrialchamber,withoutevidenceof anyattachment. (Fig.1, Videos1and 2)The mass measured 2.8×2.1 cm and occasionally obstructed the mi-tral valve orifice during diastole without passing through. In systolethe mass was pushed back in the left atrium by the mitral leaflets,thus mimicking a pinball game. There was no more evidence of thevoluminous mural thrombus documented five months before. Theanticoagulation was suspended and surgery was planned. Threedays after the patient underwent cardiac surgery for removal of atrialmass and mitral valve replacement. Exploration of the left atriumrevealed a spherical, smooth, non-pedunculated thrombus free inthe atrial cavity (Fig. 2). The mitral valve was replaced using a St.Jude Medical mechanical heart valve. Amputation of affected toeswas performed concurrently. Her postoperative course was unevent-ful. Histology confirmed that the floating mass was a thrombus, cov-ered by endothelial cells.Atrial free-floating ball thrombus wasfirst described by Woodin 1814 during an autopsy of a 15-year-old girl with mitral steno-sis [1]. Free-floating thrombi are a rare condition occurring nearlyalways in the left atrium in patients with mitral stenosis, particu-larly when atrialfibrillation is present. While patients with non-valvular atrial fibrillation usually develop thrombosis of leftappendage, thrombus located in the body of the left atrium is com-moninpatientswithmitralstenosis[2]. The existence of a muralthrombus is crucial for the formation of a free-floating thrombus.In our case, we documented a pre-existing large left atrial muralthrombus few months before the presentation. This evidencestrongly suggests that it dropped off spontaneously in the atrium,maybe facilitated by anticoagulation. In fact, the thrombus wascovered by endothelium, thus suggesting it was probably old andmore resistant to dissolution. Symptoms include heart failure andsyncope for intermittent obstruction of mitral valve and systemicembolism for fragmentation. Sudden death due to incarcerationof the thrombus into the mitral orifice has been described [3].Our patient presented with dyspnea on exertion, which couldnot be explained by the moderate valve disease, and initial gan-grene of the left toes, suggesting embolization. It is likely thatsymptoms started with detachment of thrombus from the atrialwall. Although current guidelines recommend anticoagulation inpatients with atrial thrombus and mitral stenosis[4],inthispartic-ular scenario anticoagulation may not be useful and may be poten-tially harmful. Surgery is the treatment of choice since it permitsthe removal of the mass and the treatment of underling valvedisease.Supplementary materials related to this article can be foundonline at doi:10.1016/j.ijcard.2011.12.002.

Management of Severe Mitral Stenosis During Pregnancy

A 37-year-old woman originally from Iraq was referred at 10 weeks of gestation after an abnormal result on an echocardiogram. At this time, her only symptom was intermittent palpitations. She had no recollection of previous rheumatic fever. Past obstetric history was significant for a miscarriage at 3 months of gestation a year before the current pregnancy. On examination, heart rate was 98 bpm and irregular, and blood pressure was 100/60 mm Hg. There was no jugular venous distension. Auscultation revealed a variable first heart sound, a normal second heart sound, and an opening snap with a short second heart sound to opening snap interval. A grade 3/6 diastolic rumble was heard best at the apex. The results of the remainder of the physical examination were normal. Investigations performed included an ECG (Figure 1), which showed atrial fibrillation at an average rate of 98 bpm with no evidence of right or left ventricular enlargement. An echocardiogram showed features typical of severe rheumatic mitral stenosis (MS) (Figure 2, Movies I and II in the online-only Data Supplement, and Table). Laboratory investigation results were normal. The patient was started on systemic anticoagulation (Dalteparin) and metoprolol, and was referred to the perinatology service for assessment and follow-up for the duration of pregnancy. Figure 1. Twelve-lead ECG on initial presentation showing atrial fibrillation at a rate of 98 bpm. Figure 2. Parasternal long-axis view without ( A ) and with ( B ) color Doppler assessment showing typical features of …

Right-Sided Valve Disease Deserves a Little More Respect

Historically, right-sided valvular disease has received less attention from clinicians and researchers than left-sided valve disease, in part because of a protracted latent asymptomatic period. Moreover, because tricuspid regurgitation (TR) is often due to left-sided valve disease and pulmonary regurgitation (PR) is often secondary to congenital cardiac disease, the underlying disorder rather than the valve lesion tends to dominate the clinical picture. It is increasingly recognized that right-sided valve disease is not benign and has a significant and independent impact on morbidity and mortality. Today, diagnostic techniques and appropriate management strategies for patients with right-sided valve disease are established and continually refined. In this era of increasing awareness and improved treatment options for patients with valve disease, it is important that clinicians consider the diagnosis of right-sided valve disease, understand its pathophysiology, choose appropriate confirmatory testing, and refer patients for timely intervention to prevent clinical deterioration with associated adverse consequences. This review examines the causes of right-sided valve disease and the latest diagnostic advances and treatment options for these often-neglected valve lesions. Patients with native right-sided valve disease are rarely affected by endocarditis, and indications for prophylaxis have recently changed.1 ### Tricuspid Regurgitation TR that is at least moderate in severity is most frequently “functional” in nature and by definition not related to primary tricuspid valve (TV) leaflet pathology but rather secondary to another disease process causing right ventricular (RV) dilatation, distortion of the subvalvular apparatus, tricuspid annular dilatation, or a combination of these. Furthermore, a moderate or greater degree of TR, regardless of primary origin, usually engenders additional TR as a result of the adverse hemodynamic consequence of RV volume overload. Causes of clinically significant TR are outlined in Table 1; 2 classic examples of primary tricuspid leaflet pathology are demonstrated in Figure 1. View this table: Table 1. Causes of TV …

A 48-year-old woman with dyspnoea on exertion, anemia and thrombocytopenia

Dr. Micheli: A 48-year-old woman was admitted to our hospital after a 2-month history of dyspnoea on exertion. She did not report fever, sweats, chills, chest pain or recent weight loss. Twenty years before she had undergone mitral commissurotomy for rheumatic mitral stenosis. One week before current admission, the patient was seen in the emergency department (ED) because of paroxysmal atrial fibrillation. Synchronized electrical cardioversion was performed with recover of sinus rhythm. Echocardiography showed mitral stenosis with a valve area 1 cm and mild pulmonary hypertension. Results of routine laboratory tests were normal except for anemia and thrombocytopenia (platelet count 35,000/mm, hemoglobin 11.1 g/dl). Seven months before admission, these values were in the normal range. After discharge, the patient continued to experience dyspnoea while walking for a short distance and orthopnea. Eleven years before she had undergone excision of a right breast carcinoma, and had received a 6-month cycle of adjuvant chemotherapy. No local or systemic relapse had subsequently been documented. She worked as a pianist. There was no history of allergies. She did not report diabetes mellitus, illicit drug use, smoke history, alcohol use, hypertension, dyslipidemia or family history of heart disease or cancer. She did not consume medications except propafenone that had been prescribed in the ED a few days before. On physical examination, the patient was not in acute distress. Blood pressure was 115/70 mmHg, pulse rate 98 beats/min, respiratory rate16 breaths/min, temperature 36 C and SpO2 98% while she was breathing room air. Lungs fields were clear on auscultation. A low-frequency holodiastolic murmur and mitral valve opening snap were heard over the cardiac apex. There was neither peripheral oedema nor increased jugular venous pressure. Peripheral pulses were normal and symmetrical. Abdomen was soft and non-tender. No masses or enlarged organs were detectable. There were no petechiae, ecchymoses, skin rash or lymphadenopathy. Neurologic examination was unremarkable. An electrocardiogram showed sinus rhythm. A blood gas analysis was normal. Thrombocytopenia (38,000/mm) was confirmed and pseudo-thrombocytopenia was excluded. On second hospital day, the patient abruptly developed left hemiplegia and dizziness. A CT scan of the head excluded acute intracranial hemorrhage. NIHSS was 12. The hospital Stroke Team was alerted within 30 min after the onset of symptoms but thrombolytic therapy was not performed because of the low platelet count. The patient underwent cerebral angiography that revealed diffuse bilateral microemboli not suitable for mechanical revascularization. Transesophageal echocardiography showed left appendage thrombosis. Intravenous heparin therapy S. Del Pace C. Alderighi R. Rasoini (&) R. Alterini S. Micheli G. Santoro Clinica Medica Generale e Cardiologia, Department of Heart and Vessels, Azienda Ospedaliero-Universitaria Careggi, University of Florence, Viale Morgagni 85, 50134 Florence, Italy e-mail: raffaele.rasoini@tiscali.it

Edmund H. Sonnenblick

Edmund H. Sonnenblick

Experience of the area-based dullness method of cardiac percussion in the diagnosis of cardiorespiratory disorder

Experience of the area-based dullness method of cardiac percussion in the diagnosis of cardiorespiratory disorder