Systolic Click Research Articles

Current concepts in mitral valve prolapse—Diagnosis and management

Although mitral valve prolapse as a disease entity has been recognized for over 50 years, its precise definition has been elusive. Initial reports based the diagnosis on auscultatory findings (late systolic click - murmur), with left ventricular angiography as a confirmative test. Echocardiography, first the M-mode, and subsequently the two-dimensional, became the dominant diagnostic modality. However, the early reports did not distinguish between billowing valve and flail valve. The advent of surgical repair techniques provided a different perspective; the surgical definition of mitral valve prolapse is often different from that of cardiologists. Intraoperative echocardiography gained wide acceptance necessitating a common language to describe precise terminology of the leaflet anatomy and definition of valve prolapse. The present report proposes a terminology and definitions of valve prolapse with relevance to surgical mitral valve repair. The addition of real-time 3D transesophageal echocardiography now provides highly accurate localization of lesions and the multi segment assessment of valve pathology. The etiologic considerations and surgical repair techniques with the role of echo - surgery team in improved patient outcome are described.

Uncommon variation in the papillary muscles presenting with ST elevation and T-wave inversion

A 61-year-old woman was admitted for intermittent chest discomfort that had been present for 2 months. She was normotensive and denied any past history of medical illness. On physical examination, grade 2 systolic click murmur at the left ventricular (LV) apex was auscultated. A routine electrocardiogram (Panel A) revealed ST-segment …

Digital phonocardiography as a screening tool for heart disease in childhood

To evaluate the performance of experienced cardiologists by use of digital phonocardiography for the correct identification of heart disease and innocent murmurs in children. Two independent paediatric cardiologists blindly evaluated 83 digital phonocardiograms obtained from consecutive paediatric cardiology outpatients. Each observer had to document the presence and characteristics of murmurs (intensity, quality, location), the presence of additional abnormal auscultatory findings (systolic click, second heart tone abnormalities) and whether he would recommend echocardiography (ECHO). The accuracy of their diagnoses was tested against the ECG diagnosis within two severity levels of heart disease. Twenty-three out of 24 cases (95.8%) with moderate-to-severe heart defects and 12 to 13 out of 19 cases (63.2%-68.4%) with trivial-to-mild heart defects were correctly identified by phonocardiography. Additionally, 37 to 38 out of 40 cases (92.5%-95.0%) without ECHO evidence of heart disease were correctly interpreted as having innocent murmurs. The level of agreement between the two observers was substantial regarding their recommendations for ECHO (kappa, kappa=0.83) and in identifying abnormal murmurs (kappa=0.78). Evaluation of digital phonocardiography by experienced cardiologists could allow for correct identification of moderate-to-severe forms of heart disease while preventing the majority of children with innocent murmurs from unnecessary referral.

Vegetation Stalagmite in Left Atrium

Mitral valve prolapse (MVP) is a common disorder, occurring in 4% of the general population.1 It is associated with increased risk of infective endocarditis, and antibiotic prophylaxis is suggested in those high-risk patients who have systolic murmurs.2 The vast majority of cases involve the valve and its accessory apparatus. Herein, we present an unusual location of vegetation in a patient with MVP. A 45-year-old woman had been diagnosed with MVP 1 month before admission at our institution, after a grade III/VI pansystolic murmur with late systolic click was heard during a regular health checkup. Echocardiography illustrated myxomatous change and prolapse of the anterior mitral leaflet, with severe eccentric mitral regurgitation. Because of intermittent fever, left flank pain, and tender skin erythema of both feet, the patient visited our emergency department, where blood pressure 113/76 mm Hg, heart rate 126 bpm, and body temperature 39.5°C were noted. Blood analysis showed white blood cell count of 11 400/mm3, hemoglobin level of 9.7 g/dL, C-reactive …

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.

Staphylococcus lugdunensis Prosthetic Mitral Valve Endocarditis Complicated by Paravalvular Abscess and Septic Emboli

Staphylococcus lugdunensis Prosthetic Mitral Valve Endocarditis Complicated by Paravalvular Abscess and Septic Emboli

Is mitral valve prolapse a manifestation of adolescent growth spurt?

The exact aetiology of mitral valve prolapse (MVP) is unknown, although this is the most common cardiac valvular abnormality currently detected. MVP has high incidence in young individuals, particularly during the second and third decades. These individuals are usually of a slender body habitus indicating higher rates of linear growth, reflective of the adolescent growth spurt. MVP might represent the imbalance in the growth dynamics of the mitral valve apparatus especially between the leaflets, chordae tendineae and the rest of the heart. Several reports suggest the transient nature of MVP and even complete disappearance. MVP with systolic click, but without a systolic murmur signifying regurgitation may be considered as a manifestation of adolescent growth spurt and a normal variant transiently occurring during particular periods of lives of otherwise normal individuals. Strategies of identification of subsets of individuals likely to harbor the more sinister and progressive form of MVP are important and need to be developed.

Toward an Understanding of the Cause of Mitral Valve Prolapse

Toward an Understanding of the Cause of Mitral Valve Prolapse

A Case for Routine Screening of Coronary Artery Origins During Echocardiography: Fortuitous Discovery of a Life-Threatening Coronary Anomaly

Anomalous origin of the left main coronary artery from the right sinus of Valsalva with retropulmonary course is a rare congenital abnormality. It is associated with a high incidence of sudden cardiac death, particularly among young, athletic individuals. Many of these individuals do not have symptoms before sudden death, and the diagnosis is usually made at postmortem examination. We present a case of a 15-year-old boy who was evaluated for a systolic click with routine 2-dimensional echocardiography. The anomalous coronary artery was serendipitously identified, allowing surgical intervention. Coronary artery origin and proximal course should be visualized on routine echocardiography in the pediatric population. (J Am Soc Echocardiogr 1999;12:769-72.)

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.

Incidence and risk factors for mitral valve prolapse in severe adolescent idiopathic scoliosis.

Mitral valve prolapse (MVP) is known to be associated with thoracic skeletal anomalies. To determine the incidence and risk factors for mitral valve prolapse in the adolescent population with severe idiopathic scoliosis (IS), a prospective follow-up study on 139 adolescent patients with IS from the Pediatric Orthopedic Service was undertaken. Data collected included age, sex, medical and family history, physical exam, electrocardiogram and echocardiogram, spinal x-rays, and pulmonary function tests. MVP was detected by echocardiogram in 13.6% (19/139) of patients with IS as compared with 3.2% in 154 age- and weight-matched controls (p < 0.006). All patients with MVP were asymptomatic and a systolic click or murmur was detected on the single preoperative exam only in 37% (7/19) of them. Patients with MVP and IS weighed less (45.1 +/- 2.0 vs 51.8 +/- 0.1 kg, p < 0.002) as compared with those IS patients without MVP. The electrocardiogram was abnormal in 21% (4/19) of patients with MVP as compared with only 1.6% (2/120) of patients with IS but no MVP. The two groups did not differ with respect to age at diagnosis, severity of scoliosis, positive family history of scoliosis, or the presence of restrictive lung disease. Though IS was more prevalent in females (79%), the presence of MVP was not related to gender. MVP was persistent in 10 of the 19 patients reevaluated by echocardiogram 2-4 years after spinal surgery. We conclude that MVP is four times more common in patients with severe IS than in the normal adolescent population, and is associated with a lower body weight in IS patients with MVP than in IS patients without MVP. The persistent nature of MVP, even after corrective spinal surgery, may be related to factors other than geometric changes of the heart caused by abnormal thoracic curvature.

Atrial septal aneurysm and cardiac arrhythmias

Atrial septal aneurysm has been associated with thromboembolic events, interatrial shunting, mitral valve prolapse, and systolic click. An association between atrial septal aneurysm and cardiac arrhythmias has been also described. Twenty patients with atrial septal aneurysm and 19 control subjects performed 24-h Holter monitoring. Frequent (>10/h) atrial premature beats were observed in seven patients vs. none of the controls ( P = 0.008). The mean number of episodes of supraventricular tachycardia and the prevalence of ventricular tachycardia were also higher in the atrial septal aneurysm group ( P = 0.044 and P = 0.046, respectively). Left atrial enlargement, mitral valve prolapse and left ventricular hypertrophy were more frequent than in the normal subjects. In conclusion, atrial and ventricular ‘complex’ arrhythmias occurred more frequently in patients with atrial septal aneurysm than in normal subjects. Further studies in patients with atrial septal aneurysm without other associated echocardiographic abnormalities need to be done to ascertain a potential arrhythmogenicity of this condition.

Continuous Spinal Analgesia with Sufentanil for Labor and Delivery in a Parturient with Severe Pulmonary Stenosis

Continuous Spinal Analgesia with Sufentanil for Labor and Delivery in a Parturient with Severe Pulmonary Stenosis

Anatomic explanation of mobile systolic clicks: Implications for the clinical and echocardiographic diagnosis of mitral valve prolapse

An echocardiogram (echo) is often ordered for suspected mitral valve prolapse (MVP). Using echo as the gold standard, we conducted a meticulous physical examination on 61 patients with this referral diagnosis. Ninety percent of patients with negative physical examination and echo results for MVP had physical examination findings likely to have been misinterpreted as MVP by the referring physician. Redundant portions of the mitral valve apparatus were found in 57% of patients with MVP on our physical examination but not on echo. A carefully performed physical examination (including dynamic auscultation) can exclude MVP. Not all mobile systolic clicks are associated with anatomic echo prolapse; they can be generated by redundant chordae tendineae and, in the absence of echo prolapse, probably by redundant leaflets. Patients with mobile systolic clicks should have an echo to determine the portion of the spectrum of echo prolapse present and to determine risk stratification and management.

Myths of Dental-Induced Endocarditis

We enjoyed reading Wahl's recent review article 1 on dental-induced endocarditis. His clarification of the facts about this disease was very useful. We wish to report a case of endocarditis associated with use of a home plaque removal instrument to illustrate several of his points. Report of a Case. A 62-year-old man, with previously proven mitral valve prolapse and mitral regurgitation, presented to his family physician with a 10-week history of not feeling well. In the week prior to presentation, he developed fever, chills, anorexia, and pain in the fingertips of one hand. On examination, the patient was pale, with toxic effects, and had an oral temperature of 38.2°C. Cardiac examination revealed a pulse rate of 88 beats per minute, a blood pressure level of 120/76 mm Hg, and a grade III/VI holosystolic murmur in the mitral area, with no systolic click. The heart rhythm was normal sinus, and there

Cardiac pearls

Most diagnoses of cardiovascular disease are made in the office or at the bedside. For example, in pulsus alternans of the radial pulse, observed when first greeting a patient, alteration of intensity of the second sound and systolic murmur and a ventricular (S3) gallop are clinical pearls--often subtle--that diagnose cardiac decompensation. A faint gallop, ventricular (S3) or atrial (S4), might be overlooked in a patient who has an emphysematous chest and an increase in anteroposterior diameter if one listens over the usual areas of the precordium. However, the gallop might be detected easily by listening over the xiphoid or epigastric area. How do you tell the difference between an S4, a split first sound, and an ejection sound? The S4 is eliminated with pressure on the stethoscope, but pressure does not eliminate the ejection sound or the splitting of S1. The atrial sound (S4) is most frequently found in patients who have coronary heart disease, and it is a constant finding in patients who have hypertension. It does not denote heart failure, as does the S3 (ventricular) gallop. In some patients, both atrial (S4) and ventricular (S3) diastolic gallops may be present. This occurrence is common in patients with cardiac decompensation associated with coronary heart disease, hypertensive heart disease, and dilated cardiomyopathy. When these diastolic filling sounds occur in close proximity, a short rumbling murmur may be heard, which causes confusion of this sound with that of a valvular or congenital lesion. When both sounds occur exactly simultaneously, a single sound results. Often, this sound is louder than either the first or second sound and can be misinterpreted as either a valvular or congenital lesion. This, however, is a summation gallop, which is rare. For the most accurate timing of heart sounds and murmurs, the simple technique called "inching" is the best. Keeping the second sound in mind as a reference, the physician moves (inches) the stethoscope from the aortic area to the apex. An extra sound may be noted to occur in systole before the second sound, thereby diagnosing a systolic click. If the sound occurs after the second sound, however, it is an S3 or ventricular diastolic gallop. If a murmur appears before S2, it is a systolic murmur; if it appears after S2, it is a diastolic murmur. When the Austin-Flint murmur is heard, significant aortic regurgitation exists.(ABSTRACT TRUNCATED AT 400 WORDS)

A patient with diarrhea, arthralgias, and fever

A 28-year-old carpenter presented with diarrhea and abdominal pain for the past 4 months. He reported the passage of 4-6 loose stools daily, associated with crampy midabdominal pain and bloating. He also reported a 5-year history of fever. This occurred primarily in the evenings, with temperatures sometimes reaching 103’F associated with drenching sweats. In addition, there was a 5-year history of fatigue and migratory arthralgias involving the proximal interphalangeal joints, wrists, elbows, knees, ankles, tarsal areas, and metatarsophalangeal joints. The arthralgias would usually only involve a single joint at a time with pain lasting 1-4 days in a given joint area. He had been treated with enteric-coated aspirin up to 4 g/day, as wel1 as with prednisone in a dose ranging from 5 to 10 mg daily, with excellent suppression of the arthralgias, although not complete relief of the fevers. He denied use of other medications. He was married, and there was no history of sexually transmitted disease or illicit drug use. His father was Italian and mother German; there was no family history of gastrointestina1 disease. The review of systems revealed no history of gastrointestinal bleeding, weight loss, skin rash, or other symptoms. On examination, his temperature was 36.9”C. He was muscular and healthy appearing. The vita1 signs were normal. The skin and mucous membrane examinations did not reveal any abnormalities. NO pallor or clubbing was noted. Abdominal examination revealed no masses or tenderness, and recta1 examination was normal. There were several smal1 nontender axillary nodes bilaterally and several less prominent inguinal nodes, but no cervical lymphadenopathy. On cardiac auscultation, an inconstant soft systolic click was heard, but no murmurs or rubs were detected. Neurological examination was normal. Laboratory results were as fellows (normal values in parentheses): hemoglobin, 9.1 g/dL (12.9-16.6); mean corpus9.2 X lO”/L (4.1-10.9) with normal differential; platelet count, 593 X 109/L (184-370); erythrocyte sedimentation rate, 52 mm/h (0-22); reticulocytes, 1.1% (0.6-1.8); periphera1 blood smear showed microcytic red blood cells and slight abnormalities including regenerating macrocytes, schizocytes, keratocytes and stomatocytes; hemoglobin electrophoresis normal; serum iron, 9 pg/dL (50-150); total iron binding capacity, 266 pg/dL (250-400); iron saturation, 3% (14-50); vitamin B,,, 367 ng/L (281-1079); serum folate, 7.0 pg/L (2-20); sodium, 137 mEq/L (135145); potassium, 4.9 mEq/L (3.6-4.8); calcium, 9 mg/dL (8.9-10.1); phosph orus, 4.6 mg/dL (2.5-4.5); total protein, 6.1 g/dL (6.3-7.9); glucose, 78 mg/dL (70-100); alkaline phosphatase, 159 U/L (98-25 1); aspartate aminotransferase, 25 u/L (12-31); total bilirubin, 0.4 mg/dL (0.1-1.1); direct bilirubin, 0.1 mg/dL (0.0-0.3); uric acid, 4.2 mg/dL (4.3-8.0); creatinine, 1.0 mg/dL (0.8-1.2); albumin, 3.3 g/ dL (3.5-5.0); total thyroxine, 6.5 pg/dL (5.0-12.5); fecal hemoglobin, 1.6 mg/g stool (0-2); rheumatoid factor, ~30 IU/mL (0-39); antinuclear antibody negative; anti-double stranded DNA, 53 U (0-70); and rapid plasma reagin nonreactive. Stool for parasites was negative; there were some fatty crystals. Cultures of urine and blood were negative. Chest and spine radiographs were normal. An upper gastrointestinal barium series showed a normal esophagus and stomach but minimally thickened duodenal and proximal jejunal folds. A barium enema showed slightly prominent “lymphoid follicles” in the cecum and ascending colon.

Direct visualization of left ventricular free wall rupture by transesophageal echocardiography in acute myocardial infarction

clinical significance in the majority of cases, it has been reportedly related to putative embolic events, systolic clicks, and atrial arrhythmias. 4 ASA may also masquerade as a right atrial mass. 5 The presence of ASA in our patient with symptomatic severe mitral stenosis was clearly clinically relevant, and it presented a therapeutic dilemma and challenge. In view of her young age and pliable, noncalcified mitral valve, the patient was an ideal candidate for PTMC. 6 On the other hand, PTMC requires passage of a large-caliber 12F balloon catheter across the interatrial septum, and it may thus cause extensive tear of the thin septum if atrial septal puncture is made in the fossa ovale where ASA is located. With the aid of biplane follow-through right atrial angiograms, which well delineated the relationship between the atria and ASA, puncture of the latter was avoided. The puncture was made cephalid and dorsal to the ASA, and after PTMC there was no atrial septal shunt demonstrated by oximetry or color Doppler echocardiography. The PTMC resulted in a marked improvement of the patient 's hemodynamic and clinical status.

John Barlow: mitral valve prolapse.

Although the systolic click was first mentioned in the medical literature in 1887, it was not until the investigations of John Barlow and his colleagues in the 1960s that it became linked to the mitral valve and mitral valve prolapse identified as the cause. Mitral valve prolapse is currently the most commonly diagnosed cardiac valvular abnormality. Significant complications may occur with mitral valve prolapse, though most patients are asymptomatic. However, a number of issues persist regarding mitral valve prolapse, especially with respect to the mitral valve prolapse syndrome, a term which has been applied to patients who develop a variety of symptoms, including chest pain, shortness of breath, fatigue, lightheadedness, syncope, palpitations, anxiety, and panic attacks.

Dyspnea and chest pain in a 14-year-old boy

A 14-year-old boy presented with a two-month history of dyspnea and chest pain. He also exhibited right upper quadrant tenderness, cough, and a 26 lb weight loss. On review of systems, the patient had nocturnal dyspnea and two to three pillow orthopnea. On physical exam, the patient’s lips were cyanotic and he had pallor. Examination of the heart revealed a split S2 with a systolic click. The EKG showed signs of left atria1 enlargement.