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Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

Based on our experience and the experience of others, the following classification of patients with mitral valve prolapse has been proposed. Mitral valve prolapse - Anatomic includes patients with a wide spectrum of mitral valve abnormalities from mild to severe. Symptoms, physical findings and laboratory abnormalities in these patients are directly related to mitral valve dysfunction and progressive mitral regurgitation. Complications related to abnormal mitral valve include infective endocarditis, thromboembolic events, cardiac arrhythmias, progressive mitral regurgitation, rupture of chordae tendineae and congestive heart failure. Individuals with thick mitral leaflets and mitral systolic murmur are at higher risk of developing complications. The term mitral valve prolapse syndrome refers to the occurrence of symptoms such as palpitation, chest pain, fatigue, poor exercise tolerance, dyspnea, orthostatic phenomena and syncope or presyncope in patients with mitral valve prolapse which cannot be explained on the basis of mitral valve abnormality alone. The pathogenesis of these symptoms in patients with mitral valve prolapse syndrome appears to be related to metabolic neuroendocrine abnormalities. Preventing infective endocarditis is a major consideration in patients with mitral valve prolapse. Significant mitral regurgitation with the development of congestive heart failure often requires mitral valve surgery. The most important therapeutic approach in patients with mitral valve prolapse syndrome is to explain the mechanisms of symptoms and to reassure the patient.
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PMID:Mitral valve prolapse: etiology, clinical presentation and neuroendocrine function. 134 25

A case report of the first single lung transplantation and closure of a patent ductus arteriosus for Eisenmenger's syndrome is presented. The operation was performed on Sept. 28, 1988. The patient was extubated on postoperative day 8, discharged from the intensive care unit on postoperative day 13, and discharged from the hospital on postoperative day 43, free of symptoms and without supplementary oxygen. Subsequent symptoms of dyspnea, presyncope, and fatigue recurred in association with subvalvular right ventricular outflow tract obstruction. Symptomatic improvement occurred gradually in association with reduction of the outflow tract obstruction. The patient is in New York Heart Association class I-II 12 months after the operation. The rationale, methods, and management of this patient are discussed, as well as the potential for application of this operation in similar settings.
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PMID:Single lung transplantation and closure of patent ductus arteriosus for Eisenmenger's syndrome. Toronto Lung Transplant Group. 146 29

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.
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PMID:Mitral valve prolapse syndrome: neuro-endocrinological aspects. 284 39

To define the long-term natural history of congenital complete heart block, we followed 27 patients prospectively by means of frequent ambulatory electrocardiographic (ECG) recordings for a mean (+/- SD) of 8 +/- 3 years. During that time, 8 of the 13 patients with a mean daytime heart rate below 50 bpm (Group A) had cardiac complications such as sudden death, syncope, presyncope, or excessive fatigue. Six of the eight patients had additional ECG findings that suggested an instability of the junctional escape mechanism. These findings included nocturnal junctional exit block (three patients), little or no change in the junctional rate with physical activity (three patients), and associated tachyarrhythmias (three patients). None of the 14 patients with a mean daytime heart rate of 50 bpm or more (Group B) had an adverse clinical outcome, and 5 of the 13 patients in Group A also remained well. Among the five patients in stable condition in Group A, three had no evidence of an unstable junctional mechanism. We conclude that patients with a mean daytime junctional rate below 50 bpm and other evidence of an unstable junctional escape mechanism should probably undergo prophylactic pacemaker implantation. Since junctional exit block and tachyarrhythmias sometimes appear first during follow-up, the method of risk stratification employed in this study depends on serial ambulatory ECG recordings.
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PMID:Use of ambulatory electrocardiographic monitoring to identify high-risk patients with congenital complete heart block. 382 27

Atrial fibrillation is most the common sustained arrhythmia seen by the cardiologist. Therapy to prevent this arrhythmia is often prescribed so as to eliminate associated symptoms which include palpitations, fatigue, dizziness and presyncope, shortness of breath, congestive heart failure and emboli, especially those that result in a cerebrovascular accident. Pharmacologic therapy is the only effective therapy for preventing atrial fibrillation and the class 1 antiarrhythmic drugs remain the most frequently used agents. Although each of these agents has been reported to be effective for preventing atrial fibrillation, they are associated with frequent side effects, some of which are potentially serious, especially aggravation of arrhythmia. Prior to treatment the benefit vs risk of these drugs for each patient must be established.
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PMID:Class 1 antiarrhythmic agents for therapy of atrial fibrillation. 845 55

A normal, uncomplicated pregnancy causes many physiologic cardiovascular changes and symptoms. For example, maternal blood volume, heart rate, and cardiac output increase, and fatigue, orthopnea, and presyncope often occur. In general, these findings are innocuous. Physicians need to recognize those that are not typically associated with pregnancy, such as diastolic murmurs, paroxysmal nocturnal dyspnea, and syncope. Diagnostic evaluation of pregnant women must be approached cautiously to avoid risk to the fetus. Methods using ionizing radiation should be avoided whenever possible. Hypertension, one of the most common complications of pregnancy, may be transient and benign, or it may be chronic or gestational. Early recognition and intervention are beneficial to both the mother and the child.
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PMID:Heart disease during pregnancy. Which cardiovascular changes are normal or transient? 979 64

Clinicians should be cognizant of the symptoms and risk factors associated with pulmonary hypertension (PH). While known PH poses significant therapeutic challenges, occult PH carries the added potential for unanticipated complications when treating concurrent medical illnesses. PH may occur with underlying medical conditions and risk factors or may occur de novo as idiopathic pulmonary arterial hypertension (IPAH). Symptoms of PH are frequently attributed to more common conditions, and their nonspecific nature and insidious onset may lead to delay in presentation, evaluation, and diagnosis. Initial symptoms are dyspnea, fatigue, chest pain, and palpitations. Lower extremity edema, presyncope, and syncope are symptoms of more advanced disease. Thorough evaluation of symptoms and identification of patients with risk factors for PH are critical in making a timely diagnosis. History and physical examination can identify patients with suspected PH. Further testing is necessary for definitive diagnosis, classification, assessment of severity, and guiding therapeutic decisions.
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PMID:Clinical presentation, differential diagnosis, and vasodilator testing of pulmonary hypertension. 1753 15

Inappropriate sinus tachycardia (IST) is an uncommon form of arrhythmia which is characterized by an exaggerated increase in heart rate that is out of proportion to normal physiologic demands. Usually, IST is triggered by orthostasis, minimal exertion, and psychological stress. The etiology of IST remains ill-defined. However, proposed mechanisms include: enhanced sinus node automaticity, alterations in autonomic function associated with increased sympathetic activity or reduced parasympathetic activity, and impaired baroreflex control. Recently, increased levels of autoantibodies to beta-adrenergic receptors have been observed in patients with IST. The clinical presentation of IST is highly varied and ranges from short episodes of palpitations associated with dyspnea, atypical precordial pain, cephalalgia, fatigue, and occasional syncope and presyncope to incapacitating incessant tachycardia. In general, IST is a diagnosis of exclusion. It is important that other causes of sinus tachycardia are excluded before making a diagnosis. Evaluation of autonomic function is essential for a diagnosis of IST. Treatment of IST is based on autonomic function findings and involves multidisciplinary management, including cardiac rehabilitation. Control and restitution of normal autonomic function is essential. The prognosis is benign though regular follow-up is required to optimize therapy.
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PMID:[Inappropriate sinus tachycardia: an update]. 1809 89

Postural orthostatic tachycardia syndrome was defined in adult patients as an increase >30 beats per minute in heart rate of a symptomatic patient when moving from supine to upright position. Clinical signs may include postural tachycardia, headache, abdominal discomfort, dizziness/presyncope, nausea, and fatigue. The most common adolescent presentation involves teenagers within 1-3 years of their growth spurt who, after a period of inactivity from illness or injury, cannot return to normal activity levels because of symptoms induced by upright posture. Postural orthostatic tachycardia syndrome is complex and likely has numerous, concurrent pathophysiologic etiologies, presenting along a wide spectrum of potential symptoms. Nonpharmacologic treatment includes (1) increasing aerobic exercise, (2) lower-extremity strengthening, (3) increasing fluid/salt intake, (4) psychophysiologic training for management of pain/anxiety, and (5) family education. Pharmacologic treatment is recommended on a case-by-case basis, and can include beta-blocking agents to blunt orthostatic increases in heart rate, alpha-adrenergic agents to increase peripheral vascular resistance, mineralocorticoid agents to increase blood volume, and serotonin reuptake inhibitors. An interdisciplinary research approach may determine mechanistic root causes of symptoms, and is investigating novel management plans for affected patients.
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PMID:Postural orthostatic tachycardia syndrome: a clinical review. 2011 42


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