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Válvula Aórtica/diagnóstico por imagen , Endocarditis/diagnóstico , Fluoroscopía , Sepsis/diagnóstico , Infecciones Estafilocócicas/diagnóstico , Válvula Aórtica/microbiología , Insuficiencia de la Válvula Aórtica/diagnóstico , Insuficiencia de la Válvula Aórtica/etiología , Ecocardiografía Transesofágica , Endocarditis/etiología , Humanos , Masculino , Persona de Mediana Edad , Edema Pulmonar/etiología , Insuficiencia Renal/complicaciones , Insuficiencia Renal/diagnóstico , Sepsis/etiología , Infecciones Estafilocócicas/complicacionesRESUMEN
OBJECTIVES: We hypothesized that plasma factors important for the development of atherosclerosis play a major role in the occurrence of cardiac allograft vasculopathy (CAV). BACKGROUND: Cardiac allograft vasculopathy is a major cause of death among heart transplant recipients, has a poorly understood pathogenesis and has similarities to atherosclerotic coronary disease. METHODS: The study population consisted of 93 postcardiac transplant recipients. Thirty-one patients with congestive heart failure (CHF) and 18 healthy individuals served as control subjects. Posttransplant coronary anatomy was evaluated by angiography and intravascular ultrasound. Laboratory analyses of lipids, homocysteine, vitamin B12 and folate, fibrinogen, von Willebrand factor antigen (vWFAg) and renin were obtained on all participants. RESULTS: Posttransplant patients were found to have elevated serum triglycerides, total cholesterol/ high-density lipoprotein cholesterol ratio, lipoprotein (a), homocysteine, vWFAg, fibrinogen and renin and lower high-density lipoprotein cholesterol. Most of these laboratory atherogenic factors were also elevated to a similar degree in the CHF control population. Although most atherogenic markers were elevated, there was little correlation with CAV severity. Cardiac allograft vasculopathy severity varied with time after transplantation, 3-hydroxy-methyl-glutaryl-coenzyme A reductase inhibitor use and prior cytomegalovirus infection. Even within the normal range, lower RBC folate levels were associated with increased severity of CAV. CONCLUSIONS: The posttransplant course is associated with increased clinical and laboratory atherogenic factors, some of which likely contribute to the severity of coronary vasculopathy. Compared with normal control subjects, many of these markers are already increased in pretransplant CHF patients with or without occlusive coronary artery disease.
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Arteriosclerosis/sangre , Insuficiencia Cardíaca/sangre , Trasplante de Corazón/efectos adversos , Adulto , Biomarcadores/sangre , HDL-Colesterol/sangre , LDL-Colesterol/sangre , Estudios Transversales , Femenino , Insuficiencia Cardíaca/cirugía , Homocisteína/sangre , Humanos , Masculino , Persona de Mediana Edad , Trasplante HomólogoAsunto(s)
Antígenos CD/genética , Antígenos de Plaqueta Humana/genética , Trombosis Coronaria/genética , Glicoproteínas de Membrana Plaquetaria/genética , Antígenos CD/metabolismo , Antígenos de Plaqueta Humana/metabolismo , Trombosis Coronaria/sangre , Trombosis Coronaria/etiología , Marcadores Genéticos , Genotipo , Humanos , Integrina beta3 , Integrinas/sangre , Integrinas/genética , Glicoproteínas de Membrana Plaquetaria/metabolismo , Polimorfismo Genético , Pronóstico , Recurrencia , Stents/efectos adversosRESUMEN
BACKGROUND: Although autonomic imbalance is known to be characteristics of patients with clinically overt symptomatic congestive heart failure, it is currently unknown whether this autonomic response arises early in the course of left ventricular dysfunction or is restricted to the later stages of circulatory failure. METHODS AND RESULTS: This investigation utilized the technique of spectral analysis of heart rate variability in a paced canine model of congestive heart failure that permits an examination of autonomic activity at the earliest stages of ventricular dysfunction to determine whether early systolic dysfunction in congestive heart failure is characterized by autonomic imbalance, which may contribute to subsequent myocardial and vascular dysfunction. The results indicate that autonomic imbalance as reflected in an abnormal pattern of heart rate variability evolves early in the course of ventricular systolic dysfunction consisting of both a significant increase in sympathetically influenced low-frequency heart rate variability and a significant reduction of parasympathetically mediated high-frequency variability. This was quantified by a marked and significant increase in the area under the low-frequency region from 0.053 +/- 0.037 (beats per minute)2 at baseline to 0.182 +/- 0.143 (beats per minute)2 at 48 hours to 0.253 +/- 0.202 (beats per minute)2 after 7 days of pacing (ANOVA, P < .04). The area under the high-frequency region of the curve showed a decrease from a baseline value of 0.945 +/- 0.037 (beats per minute)2 to 0.811 +/- 0.152 (beats per minute)2 at 48 hours to 0.733 +/- 0.197 (beats per minute)2 after 7 days of pacing (ANOVA, P < .03). This resulted in a shift in autonomic balance away from parasympathetic tone and toward augmented sympathetic drive as reflected by the ratio of high- to low-frequency areas from a baseline value of 15.2 +/- 9.6 to 10.1 +/- 6.89 at 48 hours and 0.004 +/- 0.001 at 7 days (ANOVA, P < .01). CONCLUSIONS: The results indicate that autonomic imbalance as reflected in an abnormal pattern of heart rate variability evolves early in the course of ventricular systolic dysfunction consisting of both a significant increase in sympathetically influenced low-frequency heart rate variability and a significant reduction of parasympathetically mediated high-frequency variability. The early appearance of these autonomic abnormalities suggests that autonomic imbalance plays a significant role in promoting the progression of circulatory failure.
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Insuficiencia Cardíaca/fisiopatología , Sistema Nervioso Parasimpático/fisiopatología , Sistema Nervioso Simpático/fisiopatología , Función Ventricular Izquierda , Animales , Modelos Animales de Enfermedad , Perros , Frecuencia Cardíaca , Ventrículos Cardíacos/inervaciónRESUMEN
BACKGROUND: Aortic input impedance is altered in patients with congestive heart failure. However, little is known about whether this vascular response is an early change or a late manifestation of left ventricular dysfunction. METHODS AND RESULTS: This investigation used a paced canine model of congestive heart failure to demonstrate that abnormal aortic input impedance does evolve in the setting of ventricular systolic dysfunction and to prospectively define the time course of change in aortic input impedance and conduit vessel compliance. Studies were performed in closed-chest conditioned beagles aged 1 to 2 years that underwent hemodynamic evaluation at baseline and after induction of left ventricular dysfunction by rapid ventricular pacing. Within 48 hours of the onset of rapid ventricular pacing, we observed mild left ventricular systolic dysfunction with an echocardiographically derived left ventricular ejection fraction of 37% (p < .001 compared with baseline) measured during interruption of rapid ventricular pacing. Concomitant with this reduction in left ventricular systolic function, the aortic input impedance spectrum was shifted above baseline in all dogs studied. Characteristic impedance of the aorta significantly increased from 121 +/- 65 dynes.s/cm5 to 186 +/- 114 dynes.s/cm5 (P < .02), and a significant increase in the first modulus of impedance from 137 +/- 43 dynes.s/cm5 to 228 +/- 139 dynes.s/cm5 was observed (P < .05). Although characteristic aortic impedance increased by 50%, there was at this point no change in peripheral vascular resistance. Therefore, these abnormalities in aortic input impedance are representative of an early vascular change that evolves in response to ventricular systolic dysfunction. CONCLUSIONS: Considering the early appearance of these findings, the resultant impaired power transfer and reduced conduit vessel compliance likely contribute to the progression of abnormal myocardial energetics and systolic dysfunction characteristic of ventricular failure.
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Aorta/fisiopatología , Insuficiencia Cardíaca/fisiopatología , Animales , Modelos Animales de Enfermedad , Perros , Insuficiencia Cardíaca/etiología , Resistencia Vascular/fisiología , Vasoconstricción/fisiología , Función Ventricular IzquierdaRESUMEN
This study describes a method for the performance of cardiac catheterization using 5 French preformed Judkins catheters from a percutaneous right brachial approach, and compares that technique to the more traditional percutaneous right femoral approach with 6 French catheters. One hundred consecutive patients requiring diagnostic left heart catheterization and selective coronary angiography were randomized according to femoral versus brachial arterial technique. Procedural efficiency, radiation exposure, and diagnostic film quality favored the femoral approach, while patient comfort, hemostasis time, time to ambulation, and decreased need for post-procedure nursing care favored the brachial approach. No differences were identified in complications. Cardiac catheterization from a right brachial artery percutaneous approach with 5 French preformed catheters has both advantages and disadvantages when compared with a more traditional femoral approach with 6 French catheters. Multiple factors should be considered before selecting an approach to diagnostic cardiac catheterization and each patient should be individually evaluated for determination of the optimal technique.
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Cateterismo Cardíaco/instrumentación , Angiografía Coronaria/instrumentación , Enfermedad Coronaria/diagnóstico por imagen , Arteria Braquial , Cineangiografía/instrumentación , Ambulación Precoz , Femenino , Arteria Femoral , Humanos , Masculino , Persona de Mediana Edad , Factores de TiempoRESUMEN
OBJECTIVES: Our objectives were to characterize by transesophageal echocardiography the normal appearance of the Starr-Edwards prosthetic heart valve and to compare the utility of transesophageal and transthoracic echocardiography in detection of valve abnormality. BACKGROUND: The Starr-Edwards prosthetic heart valve, the first mechanical valve to be used, has demonstrated excellent durability. METHODS: Fifty transthoracic and transesophageal echocardiographic studies on 37 patients with 47 Starr-Edwards prosthetic valves were analyzed retrospectively. Six cases of surgically confirmed infective endocarditis were studied. RESULTS: Vegetation or abscess formation, or both, was identified by transesophageal echocardiography in all six cases of infective endocarditis but was found in only one of these cases by transthoracic echocardiography. Thrombus was detected by transesophageal echocardiography in 9 of 11 patients with transient ischemic attacks or stroke and in 2 patients by transthoracic echocardiography with 3 confirmed at surgery. In 26 of the 30 patients with a mitral Starr-Edwards valve, the valve demonstrated a trivial or mild "closing volume" early systolic or holosystolic leak on transesophageal echocardiography alone. Transthoracic evaluation identified significant mitral regurgitation in six of the eight patients who had this finding on transesophageal echocardiography. Serial studies were performed to assess response to treatment or need for surgical intervention in eight patients. Seventeen valves have been implanted for 12 years; six of these had significant leakage without apparent cause, a finding not observed more recently implanted valves. CONCLUSIONS: These observations demonstrated the unique utility of transesophageal echocardiography in patients with Starr-Edwards prosthetic valve dysfunction, endocarditis or thrombus formation, and of the clear superiority of transesophageal echocardiography over transthoracic echocardiography in these situations.