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The formation of a thrombus in the left ventricle (LV) in patients with normal systolic function is very rare. We report a case and identified 31 other adult patients who had an LV thrombus with normal LV systolic function. The median (IQR) age of these patients was 43 [37,59] years with a slight male predominance (59%). The vast majority of patients presented with embolic complications (28; 88%) with 3 of the other patients presenting with a febrile illness. Most of the cases occurred in the setting of an identifiable medical condition that carries an increased risk of thrombosis including inflammatory diseases, malignancies or hypereosinophilia. Treatment generally included anticoagulation with or without surgical removal or systemic thrombolysis. Recurrence of LV thrombus and/or embolic events have been reported in patients with LV thrombus and normal LV systolic function suggesting that long term anticoagulation may be needed.

We present a case of simultaneous occurrence of 2 rare congenital anomalies. A 57-year-old woman undergoing evaluation of dyspnea was found to have a single coronary artery and persistent left superior vena cava. The incidence of single coronary artery is 0.024% to 0.066% in the general population. Persistent left superior vena cava occurs in 0.3% of those without other congenital anomalies and in up to 5% when other anomalies are present. The likelihood of both anomalies occurring as a random event in 1 patient is approximately 1 in 10 million. Patient characteristics and data are presented, with a discussion on the epidemiology, incidence, diagnosis and pathologic implications of each anomaly.

Myocardial bridging is a congenital abnormality characterized by an intramyocardial course of a major epicardial coronary artery segment. Generally considered a benign condition, myocardial bridging has been associated with angina, acute myocardial infarction, and sudden death. Herein, we report a patient with an intramyocardial segment in the mid portion of the left anterior descending coronary artery with marked systolic compression. Single photon emission computed tomography with technetium-99m tetrofosmin done to evaluate an episode of chest pain showed a large predominantly fixed perfusion defect in the mid to apical anterior wall with partial reversibility. The patient’s chest pain did not recur and repeat single photon emission computed tomography imaging 14 days later with rest-redistribution thallium-201 showed normal myocardial perfusion. The overall clinical impression was that myocardial bridging resulted in severe transient anterior myocardial hypoperfusion. The literature on prevalence, diagnosis, use of perfusion imaging, and hemodynamic effects of myocardial bridging is reviewed.

Coronary artery fistulae are abnormal communications between a coronary artery and a cardiac chamber or major vessel (vena cava, pulmonary veins, pulmonary artery). They are usually diagnosed by coronary arteriography. Clinical presentations are variable depending on the type of fistula, shunt volume, site of the shunt, and presence of other cardiac conditions. In this article, we review the literature regarding etiology, incidence, clinical manifestation, image studies, and management.

Background The prevalence of abdominal aneurysms has increased due to the aging population, and endovascular repair has developed into an effective, less invasive treatment. Methods/Results Two recent cases at the University of Texas-Houston highlight a variety of clinical considerations that allow informed decision-making regarding optimal treatment of abdominal aneurysms. A thorough discussion of recent data summarizes the current understanding and techniques regarding abdominal aortic aneurysm repair. Conclusions Endovascular repair of abdominal aortic aneurysms has emerged as a viable and a safe alternative to surgical repair and may offer important advantages in a majority of patients with this disease.

No-reflow is a complex condition associated with inadequate myocardial perfusion of the coronary artery in the absence of epicardial obstruction. It can occur in several settings, including percutaneous coronary intervention, especially in complex thrombotic lesions of native arteries and vein grafts and in primary angioplasty. The causes of no-reflow are not completely understood, and current treatments consist of intracoronary vasodilators, antithrombotic therapies, and mechanical devices (including aspiration thrombectomy catheters and embolic protection devices).

Tachycardia-induced cardiomyopathy occurs as a result of prolonged, excessive heart rates. Ventricular function may improve significantly upon control of the heart rate. We present a case of a patient with atrial fibrillation with rapid ventricular response who showed a dramatic improvement in left ventricular function following AV nodal ablation and insertion of a pacemaker. We also review the history and pathophysiology of tachycardia-induced cardiomyopathy.

We present a case of a patient who presented with a febrile illness without obvious source initially, who developed profound cardiac decompensation and left ventricular dysfunction. Viral titers obtained during the course of illness confirmed parvovirus infection. Intravenous aggressive immunoglobulins and medical therapy for heart failure resulted in stabilization and, ultimately, a complete recovery. Recent data from clinical trials are discussed regarding the utility of immunoglobulins in the treatment of myocarditis and heart failure.

Background Approximately 20% of cerebral infarctions are caused by a cardiac source of embolism. Although transesophageal echocardiography (TEE) is a valuable tool for evaluating patients with suspected cardioembolism, its use should be more selective. Objective We attempted to determine whether risk factors derived from the clinical, ECG, and transthoracic echocardiogram (TTE) would make TEE use more selective and increase its yield. Methods We retrospectively reviewed the records of 108 patients with suspected embolic stroke who had undergone TEE evaluation. We defined the presence of left atrial appendage spontaneous contrast (LAASC), left atrial appendage thrombus (LAAT), patent foramen ovale (PFO), or intraatrial septal aneurysm (IASA) as TEE endpoints suggestive of cardioembolism. We evaluated the association between the TEE endpoints and (1) age greater than 60 years, (2) the presence of atrial flutter (AFl) or atrial fibrillation (AF) on ECG, (3) left ventricular (LV) dysfunction by TTE (mild, LVEF 4 cm also determined by TTE. The statistical analysis performed was one-way analysis of variance controlling for interactions between different risk factors and the endpoints. Results The strongest independent predictors for the presence of LAASC or LAAT were age greater than 60 years, presence of AFl/AF, and LV systolic dysfunction. There was no association between any of the risk factors with the presence of PFO or IASA. Conclusion This study demonstrates that clinical characteristics, ECG, and TTE findings can help to better select stroke patients for TEE. Future larger studies are needed to provide more supporting data.

Prosthetic valve thrombosis is a rare but serious complication of implanted mechanical valves. Thrombolysis has emerged as an alternative to surgical therapy in the management of these patients. The indications for such therapy and appropriate patient selection are evolving. Our report describes management of a patient we encountered with this complication and reviews the current status of thrombolysis in such patients.

Aortic valve abscesses (AVAs) are a devastating complication of aortic valve endocarditis. Over 8 years, 25 patients were diagnosed with AVA by transesophageal echo (TEE). Management and outcomes were then analyzed. Eleven (44%) AVAs involved prosthetic valves, and 6 (24%) occurred in congenitally malformed valves. Twenty patients (80%) underwent surgical intervention; the rest were treated medically. Eleven (44%) of the patients died [6 (30%) surgery patients and all the medical patients]. Eight of 11 (73%) patients who died were culture positive for Staphylococcus aureus. All patients with congenitally malformed aortic valves underwent surgical intervention and survived. We conclude that: (1) despite advances in therapy and diagnosis, patients with AVAs have a high mortality rate; (2) prognosis with AVA is especially poor when S aureus is the infectious organism; (3) patients with AVAs in congenitally malformed valves have a great outcome with surgery; (4) patients treated medically have a very poor prognosis; earlier identification by TEE may be critical to improving survival.

Arterial disease involving renal, carotid, and lower extremity arteries [labeled as peripheral artery disease (PAD) for the purposes ofthis review] is increasing in frequency as the baby boomer generation ages and more patients are successfully treated for and survive longer with atherosclerotic coronary artery disease (CAD). Until the introduction of percutaneous transluminal angioplasty (PTA), surgery was the only option for treating limb ischemia, renal vascular hypertension, and carotid artery stenoses. The advent of catheter-based therapies has revolutionized therapeutic alternatives for patients with PAD. The advantages of percutaneous intervention compared with vascular surgery are reduced morbidity, diminished hospitalization time, rapid return to work, and significant cost-effectiveness. Furthermore, PTA may complement vascular surgery by increasing inflow and/or outflow so that difficult surgical procedures may be performed more successfully.

A 50-year-old male smoker with hypertension was brought to the emergency room by EMS. He reported several months of exertional chest pain. Over the previous week, the pain had increased in frequency; on the day of admission, it occurred while the patient was at rest. The last episode was accompanied by diaphoresis and shortness of breath. The patient was given nitrates in the ambulance and was pain free by the time of arrival at the emergency room. Physical examination was unremarkable. Electrocardiogram (ECG) showed nonspecific changes (Figure 1).

HCM is a heterogeneous disease with various clinical presentations. Recent advances in understanding the genetic abnormalities responsible for ventricular hypertrophy promise to improve our ability to diagnose this condition and to identify subgroups who are at the highest risk of cardiovascular mortality. Numerous difficulties remain in treating patients with HCM, including obtaining relief of symptoms and preventing SCD, but several new treatment options are currently being evaluated. In the future, randomized trials comparing the major treatment options (eg, pharmacologic therapy, myotomy/myectomy, mitral valve replacement, pacemaker implantation, and nonsurgical septal reduction) will be needed to provide guidance concerning the optimal treatment of patients with HCM.

Left ventricular hypertrophy (LVH) has been shown to be 3 times more prevalent in patients with renal artery stenosis (RAS) compared to essential hypertension, but factors that predict LVH in this population are not known. We identified 66 patients with unilateral renal artery stenosis and an interpretable electrocardiogram (ECG). LVH by either Cornell voltage-duration product or Sokolow-Lyon voltage criteria was present in 18 of the 66 patients (27%). The mean intra-aortic blood pressure was 100 +/- 14 mm Hg in patients with LVH, and 104 +/- 23 mm Hg in those without LVH (P = 0.37). The average stenosis by quantitative computerized angiography was 68 +/- 17% in patients with LVH, and 64 +/- 13% in those without LVH (P = 0.34). The mean translesional pressure gradient was 11 +/- 15 mm Hg in patients with LVH, and 13 +/- 20 mm Hg in those without LVH (P = 0.60). Using linear regression models, there was no correlation between intra-aortic blood pressure, percentage of stenosis, or translesional pressure gradient and either Cornell voltage-duration product or Sokolow-Lyon voltage criteria. In summary, LVH using ECG criteria was present in 27% of patients with unilateral RAS but was not associated with blood pressure at the time of the procedure or severity of renal artery stenosis.

One-sixth of all ischemic strokes are a result of embolization from the heart. Echocardiography serves as the cornerstone in evaluating patients who may have had a cardioembolic stroke. This article is the first of a two-part review series focusing on the role of echocardiography in the diagnosis and treatment of cardioembolic stroke. Specifically, this section will focus on nonrheumatic atrial fibrillation as well as cardiovascular masses as potential embolic sources.

The correct timing of aortic valve replacement in chronic aortic stenosis or regurgitation is a very important and sometimes difficult task for physicians caring for patients with aortic valve disease. In this review, we will present the current available literature regarding the appropriate management of these patients.

Chronic pericardial effusions are a major cause of morbidity in some clinical settings. Although the treatment of choice for acute symptomatic pericardial effusions (tamponade) is pericardiocentesis, the long-term management of symptomatic chronic pericardial effusions provides a greater challenge. The aim of this review is to provide insight into the presentation,diagnosis, and different treatment options available to patients with chronic symptomatic pericardial effusions,with emphasis on malignant pericardial effusions. Peri-cardiocentesis with sclerosing agents, radiation therapy,percutaneous, and surgical pericardiotomy and other surgical techniques are particularly efficacious, depend-ing on the underlying cause and the patient's prognosis.

M valve prolapse (MVP) is a common valvular disorder characterized by abnormalities of the mitral valve apparatus that result in “billowing” of 1 or both mitral leaflets into the left atrium during systole, with or without mitral regurgitation (MR).1–3 It is the most frequently diagnosed valve abnormality in the industrial world,4,5 and the most common primary cause for dysfunction requiring mitral valve repair or replacement.6 Clinical classification may have significant overlap and “the pathogenesis of symptoms is not completely understood.”7 The overall incidence (by echocardiography) in the Framingham study was 5%, with a frequency in women approximately twice that of men.8 Table 1 highlights the variability in the prevalence of MVP by different diagnostic methods. MVP is classified as an inheritable connective tissue disorder that is regarded as an autosomal dominant disorder with variable penetrance and is divided into primary and secondary MVP. Primary MVP accounts for the vast majority of the cases and many, but not all, of these are associated with myxomatous degeneration of the mitral valve (MV). Secondary MVP is caused by chordae tendineae rupture and/or abnormal left ventricular (LV) wall motion. Potential causes of secondary MVP include coronary artery disease, rheumatic heart disease, cardiomyopathies, and infective endocarditis.9 Also, MVP may be associated with heritable disorders such as the Marfan syndrome, the Ehlers-Danlos syndrome, and other connective tissue disorders in which myxomatous degeneration of the MV is a prominent feature. Variables that decrease LV size can worsen MVP and similarly, variables that increase LV size can mask MVP. LV size is affected by blood volume, body position (supine, standing, etc.), and maneuvers (eg, Valsalva). A decrease in LV volume is the probable cause of the increased incidence of MVP in atrial septal defect and anorexia nervosa.10–12

Controversy exists regarding the diagnostic accuracy, optimal technique, and timing of noninvasive stress testing after percutaneous transluminal coronary angioplasty (PTCA). Many patients return with chest pain after PTCA, and because the incidence of restenosis has been reported to be as high as 50%, a noninvasive test with a high predictive value is needed to reduce the need for unnecessary coronary angiography. Studies have shown that the sensitivity and specificity of stress testing varies depending on the amount of time elapsed since the procedure. Soon after a successful PTCA, perfusion defects on nuclear imaging following exercise or pharmacologic stress may be detected in asymptomatic patients without angiographic restenosis. In many patients, abnormal stress myocardial perfusion scans will normalize spontaneously, and thus stress testing with nuclear imaging within 4 to 6 weeks of PTCA lacks specificity for detecting restenosis. In contrast, stress echocardiography which detects wall motion abnormalities rather than perfusion mismatch has been reported to offer more specific information on myocardial ischemia and restenosis early after PTCA. In patients who develop chest pain more than 6 weeks after PTCA, the ability to accurately identify restenosis is shared by both echocardiographic and nuclear imaging methods. The purpose of this review is to clarify the strengths, pitfalls, and prognostic value of different stress modalities and cardiac imaging techniques in patients who develop chest pain within 6 months of undergoing PTCA.