In celebrating the 1,000th implantation of a left ventricular assist device (LVAD) at the Texas Heart Institute (THI), we find it particularly appropriate to recognize the contributions of Dr. O.H. (Bud) Frazier. As important as Bud's contributions have been to THI, they have been that much more important to the entire field of cardiac replacement therapy. Early in his career, Bud was inspired by the vision of Dr. Michael DeBakey and the energy of Dr. Denton Cooley, who pioneered mechanical circulatory support (MCS) and replacement in the 1960s. The early attempts to replace the human heart have been compared to
Genius is the very eye of intellect and the wing of thought; it is always in advance of its time, and is the pioneer for the generation which it precedes. —William Gilmore Simms Dr. O.H. “Bud” Frazier recently implanted his 1,000th ventricular assist device to help a patient with advanced heart failure. This alone is an amazing feat that is a testament to his surgical skills and the program he has developed for treating patients with advanced heart failure. Although this is monumental and worthy of recognition, it is only a small part of Dr. Frazier's contributions to the development
In the closing days of 2013, Dr. O.H. “Bud” Frazier and the Texas Heart Institute (THI) team performed their 1,000th ventricular assist device (VAD) implantation. This landmark achievement occurred barely more than half a century after Dr. Denton A. Cooley founded THI in 1962 as an institution dedicated to reducing the “devastating toll of cardiovascular disease through innovative programs in treatment, education, and research.”1 The 1,000th VAD implantation occurred almost exactly 50 years after the original 1964 National Heart Institute (NHI) grant was awarded to Dr. Michael E. DeBakey and the Baylor College of Medicine for the development
Mechanical circulatory support of the failing heart has become an important means of treating end-stage heart disease. This rapidly growing therapeutic field has produced impressive clinical outcomes and has great potential to help thousands of otherwise terminal patients worldwide. In this review, we examine the state of the art of mechanical circulatory support: current practice, totally implantable systems of the future, evolving biventricular support mechanisms, the potential for myocardial recovery and adjunctive treatment methods, and miniaturized devices with expanded indications for therapy.
Mavis Parrott Kelsey was born in Deport, Texas, on 7 October 1912. His parents owned a hardware store in rural Texas. He grew up with no electricity, running water, or sewer service until the mid-1920s. Dr. Kelsey believed that these early experiences enabled him to build discipline and toughness, all of which served him well in his later career. Dr. Kelsey's grandfather was a physician who inspired him to go into medicine. After graduating from Texas A&M College in 1932
Ray C. Fish (1902–1962) was a leading figure in Houston's natural gas industry and a philanthropist. He believed in the American dream of “opportunity for success.” The Ray C. Fish Foundation was established so that others might be encouraged to broaden man's self-knowledge and to keep the American dream alive. After its founder's death from heart disease, the Fish Foundation granted $5 million to make the Texas Heart Institute a reality. For this reason, the Institute's highest professional award is given in honor of this extraordinary man. The award recognizes
On 16 April 2002, my colleagues and I performed, in an inoperable and desperately ill man with critical calcific aortic stenosis (AS), the first clinical percutaneous implantation of an aortic valve bioprosthesis. As of 2013, more than 80,000 patients have been treated; and transcatheter aortic valve replacement (TAVR), so strongly criticized by all the experts throughout the early years, continues to grow in parallel with its constant technological improvements. Transcatheter aortic valve replacement can now be recognized as a medical breakthrough. It is a revolutionary technology that meets an unfulfilled clinical need for a common disease, is validated by rigorous
Have you called your doctor's office lately? If so, you undoubtedly hoped to speak directly with someone who might meet your need or connect you with someone who could. But to your surprise and disappointment, instead of a live person answering the telephone, a recording came on: “Thank you for calling Medical Associates, Incorporated, your friendly health-care providers. We are located at 1414 Main Street, just east of Holy Moly Hospital. Our office hours are 8 am to 5 pm, Mondays through Thursdays, with an hour for lunch from 12 to 1 pm. On
Anthropologists are known for being cultural critics and therefore are seldom invited anywhere, by anyone, for any reason. At times, however, we are asked to offer an opinion. In that regard, I recently received a note from a friend of mine—a retired cardiologist who teaches physical diagnosis at a midwestern medical school. His e-mail consisted of the
Cardiac magnetic resonance imaging has emerged as a robust noninvasive technique for the investigation of cardiovascular disorders. The coming-of-age of cardiac magnetic resonance—and especially its widening span of applications—has generated both excitement and uncertainty in regard to its potential clinical use and its role vis-à-vis conventional imaging techniques. The purpose of this evidence-based review is to discuss some of these issues by highlighting the current (Part 1, previously published) and emerging (Part 2) applications of cardiac magnetic resonance. Familiarity with the versatile uses of cardiac magnetic resonance will facilitate its wider clinical acceptance for improving the management of patients with cardiovascular disorders.
Although numerous reports describe the results of off-pump coronary artery bypass grafting (CABG) at specialized centers and in select patient populations, it remains unclear how off-pump CABG affects real-world patient outcomes. We conducted a large, multicenter observational cohort study of perioperative death and morbidity in on-pump (ON) versus off-pump (OFF) CABG. We reviewed Veterans Affairs Surgical Quality Improvement Program data for all patients (N=65,097) who underwent isolated CABG from October 1997 through April 2011 (intention-to-treat data were available from 2005 onward). The primary outcome was perioperative (30-day or in-hospital) death; the secondary outcomes were perioperative stroke, dialysis dependence, reoperation for bleeding, mechanical circulatory support, myocardial infarction, ventilator support ≥48 hr, and mediastinitis. Propensity scores calculated from age, 17 preoperative risk factors, and year of surgery were used to match 8,911 OFF with 26,733 ON patients. In the complete cohort, compared with the ON patients (n=53,468), the OFF patients (n=11,629) had less perioperative death (2.02% vs 2.53%, P=0.0012) and lower incidences of all morbidities except perioperative myocardial infarction. In the matched cohort, perioperative death did not differ significantly between OFF and ON patients (1.94% vs 2.28%, P=0.06), but the OFF group had lower incidences of all morbidities except for perioperative myocardial infarction and mediastinitis. A subgroup intention-to-treat analysis yielded similar but smaller outcome differences between the ON and OFF groups. Off-pump CABG might be associated with decreased operative morbidity but did not affect operative death, compared with on-pump CABG. Future studies should examine the effect of off-pump CABG on long-term outcomes.
This study evaluated preoperative balloon aortic valvuloplasty (BAV) as a technique to decrease aortic valve replacement (AVR) risk in patients who have severe symptomatic aortic valve stenosis with substantial comorbidity. We report the outcomes of 18 high-risk patients who received BAV within 180 days before AVR from November 1993 through December 2011. Their median age was 78 years (range, 51–93 yr), and there were 11 men (61%). The pre-BAV median calculated Society of Thoracic Surgeons Predicted Risk of Mortality (STS PROM) was 18.3% (range, 9.4%–50.7%). Preoperative left ventricular ejection fraction measured a median of 0.23 (range, 0.05–0.68), and the median aortic valve area index was 0.4 cm2/m2 (range, 0.2–0.7 cm2/m2). The median interval from BAV to AVR was 28 days (range, 1–155 d). There were no strokes or deaths after BAV; however, 4 patients (22%) required mechanical circulatory support, 3 (17%) required femoral artery operation, and 1 (6%) developed severe aortic valve regurgitation. After BAV, the median STS PROM fell to 9.1% (range, 2.6%–25.7%) (compared with pre-BAV, P <0.001). Echocardiography before AVR showed that the median left ventricular ejection fraction had improved to 0.35 (range, 0.15–0.66), and the aortic valve area index to 0.5 cm2/m2 (range, 0.3–0.7 cm2/m2) (compared with pre-BAV, both P <0.05). All patients received AVR. Operative death occurred in 2 patients (11%), and combined operative death and morbidity in 7 patients (39%). Staged BAV substantially reduces the operative risk associated with AVR in selected patients.
This prospective cross-sectional study attempted to determine both the usefulness of the serum intercellular adhesion molecule-1 (ICAM-1) as a biomarker for pulmonary artery hypertension secondary to congenital heart disease and the nature of this marker's association with catheter angiographic findings. Our study included a total of 70 male and female children, comprising 30 patients with both pulmonary artery hypertension and congenital heart disease, 20 patients with congenital heart disease alone, and 20 healthy control subjects. Levels of ICAM-1 in plasma samples from all groups were measured by the enzyme-linked immunosorbent assay method. Cardiac catheterization was also performed in all patients. The mean serum ICAM-1 levels in pediatric patients who had congenital heart disease with and without pulmonary artery hypertension were 349.6 ± 72.9 ng/mL and 312.3 ± 69.5 ng/mL, respectively (P=0.002). In healthy control subjects, the mean serum ICAM-1 level was 231.4 ± 60.4 ng/mL. According to the results of this study, the ICAM-1 level of the pulmonary artery hypertension group was significantly higher than those of the congenital heart disease group and the healthy control group. Correlation analysis showed that ICAM-1 level was correlated with systolic and mean pulmonary artery pressures (r=0.62, P=0.001; r=0.57, P=0.001)—which are 2 important values used in diagnosis of pulmonary artery hypertension. Moreover, receiver operating characteristic analysis yielded consistent results for the prediction of pulmonary artery hypertension. Therefore, we conclude that ICAM-1 has potential use as a biomarker for the diagnosis and follow-up of pulmonary artery hypertension.
In the present study of mitral valve replacement, we investigated whether complete preservation of both leaflets (that is, the subvalvular apparatus) is superior to preservation of the posterior leaflet alone. Seventy patients who underwent mitral valve replacement in our clinic were divided into 2 groups: MVR-B (n=16), in whom both leaflets were preserved, and MVR-P (n=54), in whom only the posterior leaflet was preserved. The preoperative and postoperative clinical and echocardiographic findings were evaluated retrospectively. No signs of left ventricular outflow tract obstruction were observed in either group. In the MVR-B group, no decrease was observed in left ventricular ejection fraction during the postoperative period, whereas a significant reduction was observed in the MVR-P group (P=0.003). No differences were found between the 2 groups in their need for inotropic agents or intra-aortic balloon pump support, or in cross-clamp time, duration of intensive care unit or hospital stays, postoperative development of new atrial fibrillation, or mortality rates. Bileaflet preservation prevented the decrease in left ventricular ejection fraction that usually followed preservation of the posterior leaflet alone. However, posterior leaflet preservation alone yielded excellent results in terms of decreased left ventricular diameter. Bileaflet preservation should be the method of choice to prevent further decreases in ejection fraction and to avoid death in patients who present with substantially impaired left ventricular function.
Percutaneous closure of paravalvular leaks has emerged as an alternative to repeated surgeries. Different percutaneous techniques and various devices have been used, off-label, for paravalvular leak closure. For mitral leaks, antegrade transseptal, retrograde transfemoral, and retrograde transapical techniques have been developed. In the antegrade transseptal approach, an arteriovenous guidewire loop is often created to advance the delivery sheath. In retrograde transfemoral closure, the wire in the left atrium is usually snared after transseptal puncture, to pull it from the femoral vein. The delivery sheath and closure device will subsequently be deployed from the left atrium. Each of these procedures takes time, is costly, and increases the risk of complications. We present the cases of 3 patients in whom we closed mitral paravalvular leaks by means of a retrograde transfemoral approach, with use of an Amplatzer™ Duct Occluder II device and without the construction of an arteriovenous wire loop. We think that this approach can be very useful in a specific group of patients—reducing costs, fluoroscopy times, and complications related to transseptal puncture and construction of an arteriovenous wire loop. In our institution, this reported technique is routinely used for mitral paravalvular leak closure.
Bottinor and colleagues1 present the case of a 60-year-old woman in whom massive pulmonary embolism (PE) led to cardiac arrest with pulseless electrical activity. After her successful resuscitation, she was given systemic thrombolytic therapy and survived. Ordinarily, such management and outcome would not merit an editorial, because thrombolysis is the first-line treatment in patients with PE who present with cardiogenic shock or persistent arterial hypotension.2,3 However, the case in question wasn't ordinary. Eight weeks before her PE occurred, the patient had sustained a hemorrhagic cerebrovascular accident. That event took on added significance, because any
Massive pulmonary embolism is associated with mortality rates exceeding 50%. Current practice guidelines include the immediate administration of thrombolytic therapy in the absence of contraindications. However, thrombolysis for pulmonary embolism is said to be absolutely contraindicated in the presence of recent hemorrhagic stroke and other conditions. The current contraindications to thrombolytic therapy have been extrapolated from data on acute coronary syndrome and are not specific for venous thromboembolic disease. Some investigators have proposed that the current contraindications be viewed as relative, rather than absolute, in cases of high-risk pulmonary embolism. We present the case of a 60-year-old woman in whom massive pulmonary embolism led to cardiac arrest with pulseless electrical activity. Eight weeks earlier, she had sustained a hemorrhagic cerebrovascular accident—a classic absolute contraindication to thrombolytic therapy. Despite this practice guideline, we administered tissue plasminogen activator systemically in order to save the patient's life. This therapy did not evoke intracranial bleeding, and the patient was eventually discharged from the hospital. Until guidelines specific to venous thromboembolic disease are developed, we think that the current contraindications to thrombolysis should be considered on an individual basis in patients who are at high risk of death from massive pulmonary embolism.
Apical akinesis and dilation in the absence of obstructive coronary artery disease is a typical feature of stress-induced (takotsubo) cardiomyopathy, whereas apical hypertrophy is seen in apical-variant hypertrophic cardiomyopathy. We report the cases of 2 patients who presented with takotsubo cardiomyopathy and were subsequently found to have apical-variant hypertrophic cardiomyopathy, after the apical ballooning from the takotsubo cardiomyopathy had resolved. The first patient, a 43-year-old woman with a history of alcohol abuse, presented with shortness of breath, electrocardiographic and echocardiographic features consistent with takotsubo cardiomyopathy, and no significant coronary artery disease. An echocardiogram 2 weeks later revealed a normal left ventricular ejection fraction and newly apparent apical hypertrophy. The 2nd patient, a 70-year-old woman with pancreatitis, presented with chest pain, apical akinesis, and a left ventricular ejection fraction of 0.39, consistent with takotsubo cardiomyopathy. One month later, her left ventricular ejection fraction was normal; however, hypertrophy of the left ventricular apex was newly noted. To our knowledge, these are the first reported cases in which apical-variant hypertrophic cardiomyopathy was masked by apical ballooning from stress-induced cardiomyopathy.
In takotsubo cardiomyopathy, the clinical appearance is that of an acute myocardial infarction in the absence of obstructive coronary artery disease, with apical ballooning of the left ventricle. The condition is usually precipitated by a stressful physical or psychological experience. The mechanism is unknown but is thought to be related to catecholamine excess. We present the case of a 67-year-old woman who experienced cardiogenic shock caused by takotsubo cardiomyopathy, immediately after undergoing elective direct-current cardio-version for atrial fibrillation. After a course complicated by left ventricular failure, cardiogenic shock, and ventricular tachycardia, she made a complete clinical and echocardiographic recovery. In addition to this case, we discuss the possible direct effect of cardioversion in takotsubo cardiomyopathy.
Acute pulmonary embolism is a leading cause of death during pregnancy and delivery in the United States. We describe the case of a 25-year-old woman who presented in car-diogenic shock in week 38 of her first pregnancy. After the emergent cesarean delivery of a healthy male neonate, the mother underwent immediate surgical pulmonary embolec-tomy. We confirmed the diagnosis of pulmonary embolism intraoperatively by means of transesophageal echocardiography and removed large clots from the patient's pulmonary arteries. Mother and child were doing well, 27 months later. In addition to presenting our patient's case, we discuss the other relevant reports and the options for treating massive pulmonary embolism during pregnancy.
One difficulty with external repair of left ventricular rupture after mitral valve replacement is collateral bleeding in friable myocardium adjacent to the rupture. The bleeding is caused by tension on the closing sutures, whether or not pledgets have been used. We report the case of a 69-year-old woman who underwent an uneventful mitral valve replacement. After cardiopulmonary bypass was terminated, brisk bleeding started from high in the posterior left ventricular wall, typical of a type III defect. We undertook external repair, placing a plug of Teflon felt into the cavity of the rupture and sandwiching it into place with pledgeted mattress and figure-of-8 sutures. The space occupied by the plug decreased the distance needed to obliterate the defect and thereby reduced the tension on the sutures necessary to achieve hemostasis. This simple technique enabled closure of the defect and avoided collateral tears that would have compromised an otherwise successful repair. Two years postoperatively, the patient had normal mitral valve function and no left ventricular aneurysm. In addition to reporting the patient's case, we review the types of left ventricular rupture that can occur during mitral valve replacement and discuss the various repair options.
Endovascular and open surgical repair have been used in patients with descending thoracic aortic dissection; however, the appropriate treatment is debated. We describe the case of a 60-year-old woman who had a symptomatic, chronic, residual, descending thoracic aortic dissection that was complicated by an aortobronchial fistula. She underwent emergent thoracic endovascular stent-grafting but remained symptomatic. Computed tomographic angiograms showed a contained rupture into the lower lobe of the left lung. The patient underwent definitive surgery to remove the stents, reconstruct the aorta, and resect the nonviable lung tissue. The remainder of her postoperative course was uneventful, and she was discharged from the hospital 13 days after the 2nd operation. Results of genetic testing confirmed an earlier presumptive diagnosis of Marfan syndrome. In an emergency, the best initial option for patients with a complicated descending thoracic aortic dissection might be thoracic endovascular aortic repair, which could serve as a bridge to definitive open repair.
A 55-year-old woman with a history of complete heart block, atrial flutter, and progressive right ventricular failure was referred to our tertiary care center to be evaluated for cardiac transplantation. The patient's clinical course included worsening right ventricular dysfunction for 3 years before the current evaluation. Our clinical findings raised concerns about arrhythmogenic right ventricular cardiomyopathy. Noninvasive imaging, including a positron emission tomographic scan, did not reveal obvious myocardial pathologic conditions. Given the end-stage nature of the patient's right ventricular failure and her dependence on inotropic agents, she underwent urgent listing and subsequent heart transplantation. Pathologic examination of the explanted heart revealed isolated right ventricular sarcoidosis with replacement fibrosis. Biopsy samples of the cardiac allograft 6 months after transplantation showed no recurrence of sarcoidosis. This atypical presentation of isolated cardiac sarcoidosis posed a considerable diagnostic challenge. In addition to discussing the patient's case, we review the relevant medical literature and discuss the need for updated differential diagnostic criteria for end-stage right ventricular failure that mimics arrhythmogenic right ventricular cardiomyopathy.
The human immunodeficiency virus (HIV) can cause diverse cardiovascular complications. In HIV patients on antiretroviral therapy, the prevalence of myocardial infarction has steadily increased over the years. Young patients who are naïve to antiretroviral therapy and who experience coronary events are not well represented in the medical literature. We describe the case of a 22-year-old man, infected with HIV for 4 years and never treated with antiretroviral therapy, who emergently presented with a non-ST-segment-elevation myocardial infarction. Coronary angiograms revealed thrombosis and multiple coronary artery aneurysms; however, no areas of atherosclerotic stenosis were apparent. He was successfully treated with coronary stenting, antiplatelet therapy, and anticoagulation. Nine months after the initial presentation, he exhibited excellent exercise capacity, and no ischemia was evident. We discuss the various therapeutic approaches in this case.
A 26-year-old woman, a well-trained runner, had a sudden cardiac arrest just before crossing the finish line of a marathon. She was rapidly resuscitated and was later found to have an ectopic origin of the left coronary artery. This anomaly was surgically repaired by translocating the ostium from the right to the left sinus of Valsalva. Her difficult postoperative course prompted further coronary evaluation, which revealed severe stenosis of the neoostium. The patient underwent a second operation: this time, the stenosis was bypassed via a left internal mammary artery-to-left anterior descending coronary artery (LAD) graft. Hypoplasia of the LAD and spasm during manipulation caused the graft to fail, necessitating double-stent angioplasty of the left main ostium and the LAD 2 months later. At the patient's 6-month follow-up examination, she had no further evidence of functional ischemia, and she resumed jogging. Because the mode and mechanism of the patient's condition and events were documented in unusual detail, this case furthers our understanding of sudden cardiac arrest in athletes who have rare coronary anomalies. We conclude that ectopia of a coronary artery does not itself cause potentially fatal ischemia. Rather, these events are due to the ectopic artery's intramural proximal course within the aortic media, which might result in critical stenosis by means of hypoplasia or lateral compression of the artery.
Various sequelae of alcohol septal ablation for hypertrophic obstructive cardiomyopathy have been reported. Of note, some cases of cardiac tamponade after alcohol septal ablation cannot be well explained. We describe the case of a 78-year-old woman with hypertrophic obstructive cardiomyopathy in whom cardiac tamponade developed one hour after alcohol septal ablation, probably unrelated to mechanical trauma. At that time, we noted a substantial difference in the red blood cell-to-white blood cell ratio between the pericardial effusion (1,957.4) and the peripheral blood (728.3). In addition to presenting the patient's case, we speculate that a possible mechanism for acute tamponade—alcohol-induced changes in microvascular permeability—is a reasonable explanation for cases of alcohol septal ablation that are complicated by otherwise-unexplainable massive pericardial effusions.
Although survival rates after cardiac arrest remain low, new techniques are improving patients' outcomes. We present the case of a 40-year-old man who survived a cardiac arrest that lasted approximately 3½ hours. Resuscitation was performed with strict adherence to American Heart Association/American College of Cardiology Advanced Cardiac Life Support guidelines until bedside extracorporeal membrane oxygenation could be placed. A hypothermia protocol was initiated immediately afterwards. The patient had a full neurologic recovery and was bridged from dual ventricular assist devices to a total artificial heart. On hospital day 160, he underwent orthotopic heart and cadaveric kidney transplantation. On day 179, he was discharged from the hospital in ambulatory condition. To our knowledge, this is the only reported case in which a patient survived with good neurologic outcomes after a resuscitation that lasted as long as 3½ hours. Documented cases of resuscitation with good recovery after prolonged arrest give hope for improved overall outcomes in the future.
Neisseria elongata, a common oral bacterium, has been recognized as a cause of infections such as infective endocarditis, septicemia, and osteomyelitis. Neisseria-induced infective endocarditis, although infrequently reported, typically arises after dental procedures. Without antibiotic therapy, its complications can be severe. We report the case of a 27-year-old man who presented with fever, severe dyspnea, and a leg abscess from cellulitis. An echocardiogram showed a vegetation-like echogenic structure on the septal leaflet of the patient's native tricuspid valve, and an insignificant Gerbode defect. Three blood cultures grew gram-negative, antibiotic-susceptible coccobacilli that were confirmed to be N. elongata. Subsequent DNA sequencing conclusively isolated N. elongata subsp nitroreducens as the organism responsible for the infective endocarditis. The patient recovered after 21 days of antibiotic therapy. In addition to the patient's unusual case, we discuss the nature and isolation of N. elongata and its subspecies.
We present the case of a 58-year-old woman who had large lipomatous hypertrophy of the interventricular septum, a condition that is reported very infrequently. Preoperative cardiac magnetic resonance images revealed an inhomogeneous, infiltrating mass that was suppressed in fat-suppression mode. The extensive mass was causing right ventricular dysfunction, so we excised it through a right ventricular approach. The findings on histologic analysis of the mass were consistent with lipomatous hypertrophy. The patient died of septic shock on the 28th postoperative day. In addition to the patient's case, we discuss the characteristics and diagnosis of this rare entity.
Acute myocardial infarction and acute myeloid leukemia are rarely reported as concomitant conditions. The management of ST-elevation myocardial infarction (STEMI) in patients who have acute myeloid leukemia is challenging: the leukemia-related thrombocytopenia, platelet dysfunction, and systemic coagulopathy increase the risk of bleeding, and the administration of thrombolytic agents can be fatal. We report the case of a 76-year-old man who presented emergently with STEMI, myelodysplastic syndrome, and newly recognized acute myeloid leukemia transformation. Standard antiplatelet and anticoagulation therapy were contraindicated by the patient's thrombocytopenia and by his reported ecchymosis and gingival bleeding upon admission. He declined cardiac catheterization, was provided palliative care, and died 2 hours after hospital admission. We searched the English-language medical literature, found 8 relevant reports, and determined that the prognosis for patients with concomitant STEMI and acute myeloid leukemia is clearly worse than that for either individual condition. No guidelines exist to direct the management of STEMI and concomitant acute myeloid leukemia. In 2 reports, dual antiplatelet therapy, anticoagulation, and drug-eluting stent implantation were used without an increased risk of bleeding in the short term, even in the presence of thrombocytopenia. However, we think that a more conservative approach—balloon angioplasty with the provisional use of bare-metal stents—might be safer. Simultaneous chemotherapy for the acute myeloid leukemia is crucial. Older age seems to be a major risk factor: patients too frail for emergent treatment can die within hours or days.
A 39-year-old man presented with dyspnea on exertion and was found on ausculation to have a continuous machinery-like murmur. A computed tomographic (CT) angiogram with 3-dimensional reconstruction showed a tubular patent ductus arteriosus (PDA) that measured 1.7 × 1.3 cm in diameter (Figs. 1 and 2). Given the large size of the defect, we entered the PDA with a peripheral intravascular ultrasound catheter (Volcano Corporation; San Diego, Calif ) to obtain ultrasonographic images (Fig. 3), which precisely confirmed the dimensions shown on the CT scan. Because of the defect's large size, we used an
A 39-year-old man presented with a fever of 102 °F. He had a history of viridans group streptococci (VGS) bacteremia, levo-transposition of the great vessels (also known as congenitally corrected transposition), large peri-membranous ventricular septal defect (VSD), and valvular pulmonary stenosis. Prior cardiac catheterization had shown his circulation to be well balanced, with a ratio of pulmonary blood flow to systemic blood flow of 1.4:1. Examination revealed nothing unusual except for a harsh systolic ejection murmur along the left sternal border. No emboli or immunologic phenomena were seen. The patient's white blood cell count and cell count differential were normal,
A 60-year-old woman presented with fever and shortness of breath of one week's duration. Physical examination disclosed a right-lower-quadrant abdominal mass and pretibial edema. A chest computed tomogram showed bilateral pulmonary embolism, and venous Doppler ultrasonographic imaging of the lower extremities revealed acute deep vein thrombosis (DVT) of the right common femoral vein. Abdominal ultrasonograms showed a large right ovarian mass. A 2-dimensional transthoracic echocardiogram (2D TTE) showed an echogenic mass in the atria. Two-dimensional transesophageal echocardiograms (TEE) revealed an aneurysmal interatrial septum and a large, mobile mass in the right atrium. The mass was in transit through a patent
During transthoracic echocardiography (TTE), a 77-year-old woman with exertional dyspnea was found to have large, well-defined masses adjacent to the mitral valve (Fig. 1). Spectral Doppler echocardiography revealed a mean transmitral gradient of 7 mmHg, a mitral velocity–time integral of 45 cm, and a pressure half-time of 130 ms. There was moderate mitral regurgitation, although the exact mechanism was unclear on TTE. Transesophageal echocardiography revealed that the posterior mass prevented complete leaflet apposition, resulting in regurgitation (Fig. 2A), whereas the anterior mass was not affecting leaflet motion—so no mitral regurgitation was seen there (Fig. 2B
A 38-year-old man was diagnosed with primary cardiac sarcoma involving the central cardiac structures. Echocardiography revealed that a pendular portion of the tumor intermittently obstructed the mitral orifice. Magnetic resonance imaging verified infiltration into the interventricular septum and the posterior wall of the left ventricle. A biopsy report showed moderate- to high-grade fibrosarcoma, and a positron emission tomographic–computed tomographic (PET-CT) scan ruled out metastasis. The patient consented to cardiectomy and to the placement of 2 HeartMate® II (Thoratec Corporation; Pleasanton, Calif ) continuous-flow ventricular assist devices (VADs). After the heart was excised (Fig. 1), only the
