RESUMEN
OBJECTIVES: The purpose of this study was to compare the mechanisms, predictors and outcome of patients with failed direct coronary angioplasty of the infarct-related artery with those in patients with successful direct angioplasty. BACKGROUND: Direct coronary angioplasty of the infarct-related artery, without antecedent thrombolytic therapy, is an effective treatment for patients with acute myocardial infarction. Concern has been expressed over high mortality rates in patients with failed direct infarct angioplasty. METHODS: All patients treated by angioplasty were prospectively entered into a computer data base. The characteristics and outcome of all patients with failed direct angioplasty were reviewed and compared with those of patients with successful direct angioplasty. RESULTS: Direct angioplasty was successful in 705 (94%) of 750 patients and unsuccessful in 45 (6%). Patients in the failure group were more likely to be in cardiogenic shock (22% vs. 7%, p < 0.003), to have had a previous myocardial infarction (44% vs. 28%, p < 0.03) and to have three-vessel coronary artery disease (44% vs. 23%, p < 0.003). Age, gender, ejection fraction, previous bypass surgery and diabetes mellitus were similar in both groups. Only the presence of multivessel coronary artery disease (p < 0.004) and cardiogenic shock (p < 0.025) were independent predictors of failed direct angioplasty. In-hospital death (31% vs. 4.8%, p < 0.001) and the need for emergency coronary artery bypass surgery (27% vs. 0.5%, p < 0.0001) were more frequent in patients with unsuccessful than in patients with successful direct angioplasty. Patients with failed direct angioplasty and in-hospital death usually had multiple high risk characteristics, including cardiogenic shock (50%), previous myocardial infarction (43%) and multivessel coronary artery disease (93%). CONCLUSIONS: Direct coronary angioplasty is an effective method for establishing reperfusion in acute myocardial infarction. Procedural failure is infrequent, usually occurring in patients with high risk baseline characteristics.
Asunto(s)
Angioplastia Coronaria con Balón , Mortalidad Hospitalaria , Infarto del Miocardio/mortalidad , Infarto del Miocardio/terapia , Adulto , Anciano , Anciano de 80 o más Años , Angioplastia Coronaria con Balón/métodos , Angioplastia Coronaria con Balón/mortalidad , Angioplastia Coronaria con Balón/estadística & datos numéricos , Causas de Muerte , Femenino , Humanos , Modelos Logísticos , Masculino , Persona de Mediana Edad , Missouri/epidemiología , Pronóstico , Estudios Prospectivos , Insuficiencia del Tratamiento , Resultado del TratamientoRESUMEN
A 0.038 inch perfusion wire was used to selectively administer a 24-hr infusion of urokinase into the occluded saphenous vein bypass graft of a 69-yr-old woman. Immediately following subsequent reperfusion by balloon angioplasty, she developed a hemorrhagic myocardial infarction.
Asunto(s)
Angioplastia Coronaria con Balón , Puente de Arteria Coronaria , Oclusión de Injerto Vascular/terapia , Hemorragia/inducido químicamente , Infarto del Miocardio/cirugía , Miocardio/patología , Activador de Plasminógeno de Tipo Uroquinasa/efectos adversos , Anciano , Angiografía Coronaria , Extravasación de Materiales Terapéuticos y Diagnósticos/diagnóstico por imagen , Femenino , Oclusión de Injerto Vascular/diagnóstico por imagen , Hemorragia/diagnóstico por imagen , Humanos , Infusiones Intraarteriales , Infarto del Miocardio/diagnóstico por imagen , Activador de Plasminógeno de Tipo Uroquinasa/uso terapéuticoRESUMEN
Between 1981 and 1990, 1,373 patients, aged greater than or equal to 65 years (mean 71.2 +/- 4.9), underwent 1,640 multivessel percutaneous transluminal coronary angioplasty (PTCA) procedures. Of these, 224 patients (13.6%) had a left ventricular ejection fraction less than or equal to 40%, 412 (25.1%) had prior coronary artery bypass grafting (CABG) and 48 (2.9%) had left main artery dilatation. Of the 1,640 PTCA procedures, 697 were in patients with 2-vessel disease and 943 were in patients with 3-vessel disease. A mean 3.5 lesions were dilated per patient, with an overall angiographic success rate of 96%. Complete revascularization was achieved in 857 (52%). A total of 52 patients (3.2%) had a major in-hospital complication: 27 patients (1.6%) died, 24 (1.4%) had a Q-wave myocardial infarction, and 14 (0.8%) underwent emergent CABG. Stepwise logistic regression analysis identified ejection fraction less than or equal to 40% (p less than or equal to 0.001), 3-vessel disease (p less than or equal to 0.01), female gender (p less than or equal to 0.02), and PTCA between 1981 and 1985 (p less than or equal to 0.05) as independent predictors of mortality. Of the 1,373 patients, 1,023 have been followed for greater than or equal to 1 year (mean follow-up 32.5 +/- 21.3 months). There were 156 (15.2%) late deaths, 81 (7.9%) recurrent myocardial infarctions, and 162 (15.8%) coronary artery bypass operations. Actuarial survival, computed from the time of hospital discharge, was 92% at 1 year, 86% at 3 years and 78% at 5 years. Repeat PTCA was required in 371 patients (36.3%).(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Angioplastia Coronaria con Balón , Enfermedad Coronaria/terapia , Anciano , Anciano de 80 o más Años , Angioplastia Coronaria con Balón/efectos adversos , Puente de Arteria Coronaria , Circulación Coronaria , Enfermedad Coronaria/mortalidad , Femenino , Estudios de Seguimiento , Humanos , Masculino , Análisis Multivariante , PronósticoRESUMEN
To examine the effects of beta-adrenergic blockade on neurohormonal activation in patients with congestive heart failure, 15 men had assessments of hemodynamics and supine peripheral renin and norepinephrine levels before and after 3 months of oral therapy with bucindolol, a nonselective beta antagonist. At baseline, plasma renin activity did not correlate with any hemodynamic parameter. However, norepinephrine levels had a weak correlation with left ventricular end-diastolic pressure (r = 0.74, p less than 0.01), stroke volume index (r = 0.61, p less than 0.02) and pulmonary vascular resistance (r = 0.54, p less than 0.05). Plasma renin decreased with bucindolol therapy, from 11.6 +/- 13.4 to 4.3 +/- 4.1 ng/ml/hour (mean +/- standard deviation; p less than 0.05), whereas plasma norepinephrine was unchanged, from 403 +/- 231 to 408 +/- 217 pg/ml. A wide diversity of the norepinephrine response to bucindolol was observed with reduction of levels in some patients and elevation in others. Although plasma norepinephrine did not decrease, heart rate tended to decrease (from 82 +/- 20 vs 73 +/- 11 min-1, p = 0.059) with beta-adrenergic blockade, suggesting neurohormonal antagonism at the receptor level. No changes in I-123 metaiodobenzylguanidine uptake occurred after bucindolol therapy, suggesting unchanged adrenergic uptake of norepinephrine with beta-blocker therapy. Despite reductions in plasma renin activity and the presence of beta blockade, the response of renin or norepinephrine levels to long-term bucindolol therapy did not predict which patients had improved in hemodynamic status (chi-square = 0.37 for renin, 0.82 for norepinephrine).(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Antagonistas Adrenérgicos beta/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Hemodinámica/efectos de los fármacos , Norepinefrina/sangre , Propanolaminas/uso terapéutico , Renina/sangre , 3-Yodobencilguanidina , Adulto , Corazón/diagnóstico por imagen , Insuficiencia Cardíaca/diagnóstico por imagen , Humanos , Radioisótopos de Yodo , Yodobencenos , Masculino , Persona de Mediana Edad , Cintigrafía , Sistema Renina-Angiotensina/efectos de los fármacos , Sistema Nervioso Simpático/efectos de los fármacosRESUMEN
Cyclic coronary artery flow variations with a spontaneous decline in coronary blood flow to very low levels have been documented in stenosed canine coronary arteries with endothelial injury. These flow variations are associated with transient platelet aggregation and dislodgment and the release of selected mediators, including thromboxane A2 and serotonin. However, cyclic or spontaneous flow variations have not been demonstrated in stenosed coronary arteries in humans. In this study, the hypothesis was tested that spontaneous coronary blood flow velocity variations occur in some patients with stenosed coronary arteries before or after coronary artery angioplasty. Thus, 13 patients with severe and limiting angina underwent intracoronary pulsed Doppler velocimetry of their dilated artery immediately before and after percutaneous transluminal coronary angioplasty, whereas 9 control patients underwent velocimetry of an angiographically normal coronary artery. A 3F catheter with a 20 MHz Doppler crystal was positioned to achieve a maximal stable signal, and the flow velocity signal was recorded continuously for 20 min. Spontaneous flow velocity variations (greater than or equal to 38% change in Doppler frequency shift with wide morphologic changes) were present in 3 of the 13 patients tested. Spontaneous flow velocity variations occurred before angioplasty in one patient, after angioplasty in another and both before and after angioplasty in a third. In addition, 2 of the 13 patients, 1 with spontaneous coronary artery flow velocity variations before angioplasty, had frank vasospasm in an adjacent area just distal to the area of coronary dilation immediately after balloon inflation. These data establish that spontaneous coronary artery flow velocity variations occur in some patients with severe and limiting angina before and after coronary angioplasty. These variations may be related to platelet aggregation or coronary vasoconstriction, or both, at sites of endothelial injury resulting from plaque fissuring or ulceration and endothelial and medial injury occurring during coronary angioplasty.
Asunto(s)
Angina de Pecho/fisiopatología , Angioplastia Coronaria con Balón , Circulación Coronaria/fisiología , Angina de Pecho/diagnóstico por imagen , Angina de Pecho/terapia , Velocidad del Flujo Sanguíneo/fisiología , Vasos Coronarios/diagnóstico por imagen , Vasos Coronarios/fisiopatología , Humanos , Masculino , Persona de Mediana Edad , Agregación Plaquetaria , Ultrasonografía , Vasoconstricción/fisiologíaRESUMEN
STUDY OBJECTIVE: According to the Gorlin hydraulic orifice equation, aortic regurgitation volume can be determined by the regurgitant orifice cross sectional area, diastolic filling period, mean pressure gradient between the aorta and left ventricle, and a constant relating the coefficients of contraction (Cc) and velocity (Cv). This study was performed to determine whether variation in aortic valve morphology affects regurgitant flow volume, Cc and Cv. DESIGN: Four aortic valve templates, modelled after circular, rheumatic, degenerative, and bicuspid lesions, were constructed with equal orifice cross sectional areas in two sizes, 0.2 and 0.7 cm2. These valves were studied in vitro in a flow model of aortic regurgitation, wherein aortic pressure was regulated by varying the height of a column of fluid. Flow, pressure, and velocity were measured, and the coefficient Cc and Cv were calculated from standard equations. MEASUREMENTS AND MAIN RESULTS: Regurgitant volume was assessed at diastolic filling periods of 0.5 and 1.0 s and averaged 15% greater for bicuspid and degenerative as compared to circular or rheumatic valve shapes (p = 0.0001). This difference was accentuated at the shorter diastolic filling time and higher pressure gradient, such that bicuspid lesions allowed 29% more regurgitant flow across the 0.2 cm2 orifice at fluid height of 120 cm over 0.5 s. This difference in regurgitant volume between valve shapes was due to an increased Cc for the bicuspid and degenerative valve shapes, suggesting that they are more efficient orifices than rheumatic or circular valve shapes. CONCLUSIONS: Aortic valve morphology influences regurgitant volume in aortic regurgitation. Specifically, degenerative and bicuspid orifice shapes have a higher contraction coefficient and allow more regurgitant flow than rheumatic or circular orifices at a given driving pressure and diastolic filling time.
Asunto(s)
Insuficiencia de la Válvula Aórtica/patología , Válvula Aórtica/patología , Insuficiencia de la Válvula Aórtica/fisiopatología , Velocidad del Flujo Sanguíneo/fisiología , Presión Sanguínea , Humanos , Métodos , Modelos Cardiovasculares , Contracción Miocárdica/fisiologíaRESUMEN
Vasoactive intestinal peptide (VIP) is a neurotransmitter that has been identified in epicardial coronary arteries. To evaluate the direct effect of VIP on coronary hemodynamics and blood flow, graded doses of VIP (0.01, 0.03, 0.10, and 0.30 micrograms/min) were infused into the left coronary artery of 7 patients at the time of diagnostic cardiac catheterization for chest pain syndromes. None of the patients had coronary stenoses greater than 50% during subsequent angiography. Coronary sinus VIP concentrations increased during each infusion (22 +/- 28 pg/ml at baseline to 109 +/- 22 pg/ml at 0.30 micrograms/min; p less than 0.05), but arterial VIP was elevated (39 +/- 29 pg/ml) only at the maximal dose of 0.30 micrograms/min. During all dosages of VIP, heart rate, right atrial and left ventricular end-diastolic pressure, and the heart rate x blood pressure product did not change. Moreover, neither mean aortic pressure nor left ventricular peak + dP/dt changed significantly at doses less than 0.30 micrograms/min; at 0.30 micrograms/min, mean aortic pressure decreased (97 +/- 15 to 90 +/- 15 mm Hg; p less than 0.05) and LV peak + dP/dt increased (1,621 +/- 230 to 1,801 +/- 226 mm Hg/s; p less than 0.05). Compared to baseline, the arterial-coronary sinus O2 content difference and myocardial O2 extraction diminished progressively at the 0.03, 0.10, and 0.30 micrograms/min doses of VIP (118 +/- 12 ml O2/L vs. 94 +/- 15, 70 +/- 9, and 61 +/- 26 ml O2/L, respectively, and 0.64 +/- 0.05 vs. 0.53 +/- 0.10, 0.38 +/- 0.06, and 0.34 +/- 0.15, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Circulación Coronaria/efectos de los fármacos , Péptido Intestinal Vasoactivo/farmacología , Adulto , Anciano , Cateterismo Cardíaco , Vasos Coronarios , Corazón/efectos de los fármacos , Humanos , Infusiones Intravenosas , Masculino , Persona de Mediana Edad , Tono Muscular/efectos de los fármacos , Músculo Liso Vascular/efectos de los fármacos , Consumo de Oxígeno/efectos de los fármacos , Péptido Intestinal Vasoactivo/administración & dosificación , Vasodilatación/efectos de los fármacosRESUMEN
The hemodynamic effects of beta-adrenergic blockade with bucindolol, a nonselective beta-antagonist with mild vasodilatory properties, were studied in patients with congestive heart failure. Fifteen patients (New York Heart Association class I-IV) underwent cardiac catheterization before and after 3 months of oral therapy with bucindolol. The left ventricular ejection fraction increased from 0.23 +/- 0.12 to 0.29 +/- 0.14 (p = 0.007), and end-systolic elastance, a relatively load-independent determinant of contractility, increased from 0.60 +/- 0.40 to 1.11 +/- 0.45 mm Hg/ml (p = 0.0049). Both left ventricular stroke work index (34 +/- 13 to 47 +/- 19 g-m/m2, p = 0.0059) and minute work (5.5 +/- 2.2 to 7.0 +/- 2.6 kg-m/min, p = 0.0096) increased despite reductions in left ventricular end-diastolic pressure (19 +/- 8 to 15 +/- 5 mm Hg, p = 0.021). There was an upward shift in the peak + dP/dtmax-end-diastolic volume relation (p = 0.0005). These data demonstrate improvements in myocardial contractility after beta-adrenergic blockade with bucindolol. At a matched paced heart rate of 98 +/- 15 min-1, the time constant of left ventricular isovolumic relaxation was significantly reduced by bucindolol therapy (92 +/- 17 versus 73 +/- 11 msec, p = 0.0013), and the relation of the time constant to end-systolic pressure was shifted downward (p = 0.014) with therapy. The slope of the logarithm left ventricular end-diastolic pressure-end-diastolic volume relation was unchanged (p = 0.51) after bucindolol. These data suggest that chronic beta-adrenergic blockade with bucindolol improves diastolic relaxation but does not alter myocardial chamber stiffness. Myocardial oxygen extraction, consumption, and efficiency were unchanged despite improvement in contractile function and mechanical work. Thus, in patients with congestive heart failure, chronic beta-adrenergic blockade with bucindolol significantly improves myocardial contractility and minute work, yet it does not do so at the expense of myocardial oxygen consumption. Additionally, bucindolol improves myocardial relaxation but does not affect chamber stiffness.
Asunto(s)
Antagonistas Adrenérgicos beta/uso terapéutico , Insuficiencia Cardíaca/tratamiento farmacológico , Corazón/fisiopatología , Miocardio/metabolismo , Propanolaminas/uso terapéutico , Adulto , Circulación Coronaria/efectos de los fármacos , Diástole , Metabolismo Energético/efectos de los fármacos , Insuficiencia Cardíaca/metabolismo , Insuficiencia Cardíaca/fisiopatología , Hemodinámica/efectos de los fármacos , Humanos , Masculino , Persona de Mediana Edad , Contracción Miocárdica/efectos de los fármacos , Consumo de Oxígeno/efectos de los fármacosRESUMEN
STUDY OBJECTIVE: To determine whether beta-adrenergic blockade augments cocaine-induced coronary artery vasoconstriction. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: A cardiac catheterization laboratory in an urban teaching hospital. PATIENTS: Thirty clinically stable patient volunteers referred for catheterization for evaluation of chest pain. INTERVENTIONS: Heart rate, arterial pressure, coronary sinus blood flow (by thermodilution), and epicardial left coronary arterial dimensions were measured before and 15 minutes after intranasal saline or cocaine administration (2 mg/kg body weight) and again after intracoronary propranolol administration (2 mg in 5 minutes). MEASUREMENTS AND MAIN RESULTS: No variables changed after saline administration. After cocaine administration, arterial pressure and rate-pressure product increased; coronary sinus blood flow fell (139 +/- 28 [mean +/- SE] to 120 +/- 20 mL/min); coronary vascular resistance (mean arterial pressure divided by coronary sinus blood flow) rose (0.87 +/- 0.10 to 1.05 +/- 0.10 mm Hg/mL.min); and coronary arterial diameters decreased by between 6% and 9% (P less than 0.05 for all variables). Subsequently, intracoronary propranolol administration caused no change in arterial pressure or rate-pressure product but further decreased coronary sinus blood flow (to 100 +/- 14 mL/min) and increased coronary vascular resistance (to 1.20 +/- 0.12 mm Hg/mL.min) (P less than 0.05 for both). CONCLUSIONS: Cocaine-induced coronary vasoconstriction is potentiated by beta-adrenergic blockade. Beta-adrenergic blocking agents probably should be avoided in patients with cocaine-associated myocardial ischemia or infarction.
Asunto(s)
Antagonistas Adrenérgicos beta/farmacología , Cocaína/farmacología , Vasos Coronarios/efectos de los fármacos , Adulto , Anciano , Presión Sanguínea/efectos de los fármacos , Circulación Coronaria/efectos de los fármacos , Enfermedad Coronaria/fisiopatología , Método Doble Ciego , Sinergismo Farmacológico , Femenino , Humanos , Masculino , Persona de Mediana Edad , Miocardio/metabolismo , Consumo de Oxígeno/efectos de los fármacos , Propranolol/farmacología , Distribución Aleatoria , Vasoconstricción/efectos de los fármacosRESUMEN
For the detection of left-to-right intracardiac shunting, the oximetric and standard indocyanine green techniques are relatively insensitive, in that neither can reliably detect a shunt with a ratio of pulmonary to systemic flow (Qp/Qs) less than 1.3 (percentage shunt, 23%). Although the hydrogen inhalation method is said to be much more sensitive in this regard, no previous study has measured its sensitivity. Accordingly, in 15 patients (4 men, 11 women, aged 38 to 67 years) without intracardiac shunting, hydrogen inhalation was performed 1) without and 2) with an artificially created femoral arteriovenous shunt of known size, and cardiac output was measured by thermodilution. For the 15 subjects with cardiac outputs of 3.64 to 8.10 liters/min, shunts of 22 to 248 ml/min were created, so that the shunts ranged from 0.5% to 3.3%. Hydrogen inhalation detected all shunts greater than or equal to 1.3% (Qp/Qs greater than or equal to 1.01). Of the 10 shunts less than 1.3%, it detected 5, with the smallest being 0.7%. Thus, the hydrogen inhalation technique is extremely sensitive in identifying the presence of left-to-right shunting, far more sensitive than the oximetric and standard indocyanine green methods.
Asunto(s)
Cateterismo Cardíaco , Defectos de los Tabiques Cardíacos/diagnóstico , Hidrógeno , Adulto , Anciano , Gasto Cardíaco , Circulación Coronaria/fisiología , Femenino , Humanos , Técnicas de Dilución del Indicador , Verde de Indocianina , Masculino , Persona de Mediana Edad , Oximetría , TermodiluciónRESUMEN
To determine whether the asynchronous left ventricular contraction-relaxation sequence that exists during right ventricular pacing alters left ventricular relaxation, measurements of both the maximal rate of decline of left ventricular pressure (peak negative dP/dt) and the time constant of left ventricular relaxation were obtained during atrial and atrioventricular (AV) pacing in 25 patients referred for diagnostic cardiac catheterization. Heart rate was maintained at 10 to 15 beats/min above the sinus rate at rest, and relaxation was assessed during atrial pacing, AV pacing and repeat atrial pacing. The patients were classified into two groups. Group 1 included 10 patients with normal left ventricular systolic function at rest (ejection fraction greater than 0.55) and without evidence of prior myocardial infarction. Group 2 included 15 patients with a depressed left ventricular ejection fraction or akinesia of one or more left ventricular segments on the contrast ventriculogram, or both. Heart rate, peak left ventricular systolic pressure, end-systolic pressure and end-diastolic pressure remained constant during atrial, AV pacing and repeat atrial pacing in all patients. In group 1 patients, the decrease in peak negative dP/dt (1,507 +/- 200 versus 1,424 +/- 187 mm Hg/s) and the increase in the time constant of left ventricular relaxation (48 +/- 11 versus 51 +/- 11 ms) during AV pacing was not significantly different when compared with values during atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Estimulación Cardíaca Artificial , Contracción Miocárdica , Anciano , Ecocardiografía , Cardiopatías/fisiopatología , Humanos , Persona de Mediana Edad , Estudios ProspectivosRESUMEN
The effects of isradipine, a new dihydropyridine calcium antagonist, were evaluated in 24 patients referred for elective cardiac catheterization because of suspected coronary artery disease. Hemodynamics and left ventricular (LV) function (by digital subtraction angiography) were measured at baseline and during rapid atrial pacing (mean peak heart rate 135 beats/min), which induced chest pain or electrocardiographic changes in all patients. After a control pacing period, intravenous isradipine (0.01 mg/kg, n = 16) or placebo (n = 8) was administered in a double-blind fashion and all variables were measured again at baseline and during pacing to the same maximum heart rate. Before isradipine was given, pacing had no effect on systolic blood pressure, while increasing diastolic blood pressure (68 +/- 8 to 87 +/- 11 mm Hg, p less than 0.0001) and LV end-diastolic pressure measured in the immediate postpacing period (13 +/- 5 to 18 +/- 6 mm Hg, p less than 0.03) and decreasing LV end-diastolic volume index (59 +/- 18 to 40 +/- 12 ml/m2, p less than 0.001), stroke volume index (37 +/- 11 to 23 +/- 10 ml/m2, p less than 0.0001), ejection fraction (0.64 +/- 0.07 to 0.53 +/- 0.12, p less than 0.0003) and percent regional shortening in 4 of 5 myocardial wall segments. During pacing after isradipine, systolic and diastolic blood pressures were lower, ejection fraction was higher and percent regional shortening decreased in only 2 of 5 myocardial segments. In comparison to placebo, isradipine increased baseline heart rate, ejection fraction and stroke volume index while it decreased arterial pressure and end-systolic volume index before the second pacing period.(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Estimulación Cardíaca Artificial , Enfermedad Coronaria/fisiopatología , Corazón/fisiopatología , Piridinas/farmacología , Bloqueadores de los Canales de Calcio/farmacología , Estimulación Cardíaca Artificial/métodos , Corazón/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Ventrículos Cardíacos , Humanos , Infusiones Intravenosas , Isradipino , Masculino , Placebos , Factores de TiempoRESUMEN
This study was designed to determine the changes in the heart that result from inhibition of long-chain fatty acid oxidation with 2-tetradecylglycidic acid (TDGA). Male Sprague-Dawley rats (n = 64) were treated with TDGA (20 mg.kg-1.day-1) or a comparable volume of vehicle by gavage feeding for 7 or 21 days. In conscious rats TDGA produced no changes in heart rate, left ventricular systolic or end-diastolic pressures, left ventricular pressure development (dP/dt), or the time constant of left ventricular relaxation. Left ventricular developed pressure was not changed at 21 days. TDGA increased left ventricular weight, left ventricular weight-to-body weight ratio, and total heart weight-to-body weight ratio. Left ventricular endocardial and epicardial myocyte volumes were increased by 53 and 65%, respectively. Myocardial triglyceride content was increased threefold. Left ventricular chamber stiffness constants between end-diastolic pressures of 0 and 30 mmHg were increased, and left ventricular end-diastolic volumes at operating end-diastolic pressures were decreased at both 7 and 21 days. The myocardial stiffness constant was also increased at 7 and 21 days. Thus inhibition of long-chain fatty acid oxidation with TDGA increased left ventricular mass and altered left ventricular chamber and muscle stiffness without changing left ventricular relaxation or systolic function. We conclude that inhibition of long-chain fatty acid oxidation produced an unusual model of left ventricular hypertrophy and diastolic dysfunction characterized by abnormalities of passive-elastic properties but preserved relaxation.
Asunto(s)
Ácidos Grasos/antagonistas & inhibidores , Modelos Cardiovasculares , Animales , Cardiomegalia/inducido químicamente , Cardiomegalia/metabolismo , Cardiomegalia/patología , Compuestos Epoxi/farmacología , Ácidos Grasos/metabolismo , Ácidos Grasos/farmacología , Hemodinámica , Masculino , Microscopía Electrónica , Miocardio/patología , Oxidación-Reducción , Ratas , Ratas Endogámicas , Factores de TiempoRESUMEN
Doppler measurements of the velocity and acceleration of ascending aortic blood flow have been used as indexes of left ventricular (LV) contractility. Conflicting data exist, however, on the influence of LV loading conditions on these measurements. Therefore, simultaneous LV micromanometer pressure measurements, 2-dimensional echocardiography and continuous-wave Doppler studies were performed before and after preload or afterload manipulation in 16 patients with coronary artery disease. Nitroprusside (n = 9) was administered in combination with saline to maintain preload and achieve a 10 to 20% reduction in mean aortic pressure. Saline (n = 7) was administered (850 +/- 240 ml) to increase LV end-diastolic pressure 25 to 50%. All measurements were obtained during atrial pacing at a heart rate 10 to 15 beats/min above resting sinus rate. The administration of nitroprusside plus saline decreased LV end-systolic wall stress (94 +/- 27 to 67 +/- 14 g/cm2 X 10(3), p = 0.011) without changing LV end-diastolic pressure and end-diastolic dimension. Peak velocity (0.8 +/- 0.2 to 0.9 +/- 0.3, p = 0.044), velocity time integral (11 +/- 4 to 13 +/- 5 cm, p = 0.049) and mean acceleration (12 +/- 4 to 17 +/- 7 m/s2, p = 0.0014) increased significantly. The administration of saline alone significantly increased LV end-diastolic pressure (10 +/- 4 to 22 +/- 4 mm Hg, p = 0.0006), LV end-diastolic dimension (4.8 +/- 0.5 to 5.1 +/- 0.5 cm, p = 0.0001), peak velocity (0.9 +/- 0.3 to 1.0 +/- 0.4 m/s, p = 0.008), velocity-time integral (14 +/- 5 to 18 +/- 7 cm, p = 0.005), and mean acceleration (14 +/- 6 to 17 +/- 7 m/s2, p = 0.041). Thus, even a modest change in either preload or afterload altered peak velocity, the velocity time integral and mean acceleration. These data have important clinical implications regarding the application of Doppler aortic flow indexes in the assessment of LV function.
Asunto(s)
Enfermedad Coronaria/fisiopatología , Adulto , Velocidad del Flujo Sanguíneo/efectos de los fármacos , Velocidad del Flujo Sanguíneo/fisiología , Presión Sanguínea/efectos de los fármacos , Angiografía Coronaria , Enfermedad Coronaria/tratamiento farmacológico , Ecocardiografía Doppler , Hemodinámica/efectos de los fármacos , Humanos , Masculino , Persona de Mediana Edad , Contracción Miocárdica/efectos de los fármacos , Nitroprusiato/farmacología , Estudios Prospectivos , Cloruro de Sodio , UltrasonografíaRESUMEN
INTRODUCTION: This study was done to assess the accuracy and reliability of the thermodilution technique in measuring cardiac output in patients with tricuspid regurgitation. PATIENTS AND METHODS: In 30 subjects (17 men, 13 women, aged 50 +/- 14 [mean +/- SD] years), cardiac output was measured in close temporal proximity by thermodilution as well as Fick or indocyanine green dye, after which the presence and severity of tricuspid regurgitation were assessed by contrast right ventriculography or pulsed Doppler echocardiography. RESULTS: In the 13 patients without tricuspid regurgitation, there was excellent agreement between the results of thermodilution and Fick or indocyanine green dye cardiac output determinations (4.95 +/- 1.19 liters/minute by thermodilution, 4.90 +/- 1.11 liters/minute by Fick or indocyanine green dye; NS). In contrast, in the 17 patients with tricuspid regurgitation, the results of thermodilution were consistently lower than those of Fick or indocyanine green dye (4.22 +/- 1.45 liters/minute by thermodilution, 4.99 +/- 1.67 liters/minute by Fick or indocyanine green dye; p less than 0.001). CONCLUSION: Thus, the thermodilution technique of measuring cardiac output is inaccurate in patients with tricuspid regurgitation, yielding results that are consistently lower than the actual outputs.
Asunto(s)
Gasto Cardíaco , Termodilución , Insuficiencia de la Válvula Tricúspide/fisiopatología , Adulto , Anciano , Medios de Contraste , Ecocardiografía , Femenino , Humanos , Técnicas de Dilución del Indicador , Verde de Indocianina , Masculino , Persona de Mediana Edad , Radiografía , Termodilución/métodos , Insuficiencia de la Válvula Tricúspide/diagnóstico , Insuficiencia de la Válvula Tricúspide/diagnóstico por imagenRESUMEN
This study was designed to determine whether thyroid hormone (T4) produces cardiac hypertrophy and alters ventricular function by direct effects on the heart or by alterations in adrenergic stimulation or changes in the peripheral circulation. Rats were treated with captopril (4 mg/ml of drinking water), propranolol (0.5 mg/ml of drinking water), hydralazine (80 mg/l of drinking water) or the combination of captopril and propranolol with and without T4 (15 micrograms/100 g b.w. i.p.). After 10 days, T4 increased (P less than .01) heart rate, left ventricular (LV) dP/dt and LV weight/body weight, but did not alter LV systolic pressure (SP) or enddiastolic pressure (EDP). Compared to treatment with T4 alone, captopril plus T4 decreased LV SP (P less than .05) and LV EDP (P less than .01); however, heart rate, LV dP/dt and LV weight/body weight were unchanged. Treatment with T4 plus propranolol decreased heart rate and LV EDP (P less than .05) compared to T4 alone; however, LV SP, LV dP/dt and LV weight/body weight were unchanged (P greater than .05). Hydralazine did not alter (P greater than .05) heart rate, LV SP, LV EDP or prevent the development of increased LV weight/body weight when given with T4; however, LV dP/dt was slightly decreased (P less than .05). Treatment with the combination of captopril and propranolol did not alter (P greater than .05) heart rate, LV SP, LV EDP or LV dP/dt and also failed to prevent the development of increased LV weight/body weight and LV dP/dt when given with T4.(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Cardiomegalia/inducido químicamente , Receptores Adrenérgicos beta/efectos de los fármacos , Hormonas Tiroideas/farmacología , Animales , Captopril/farmacología , Corazón/efectos de los fármacos , Corazón/fisiopatología , Hidralazina/farmacología , Isoenzimas/análisis , Masculino , Miosinas/análisis , Propranolol/farmacología , Ratas , Ratas EndogámicasRESUMEN
Pneumopericardium and hydropneumopericardium are rare conditions in which hemodynamic compromise is common. Loss of the M-mode and two-dimensional image coincident with the systolic phase of each cardiac cycle and swirling echogenic bubbles within the pericardial space produce a distinctive M-mode and two-dimensional echocardiographic appearance. This provides an additional method for prompt diagnosis.
Asunto(s)
Ecocardiografía , Derrame Pericárdico/diagnóstico , Neumopericardio/diagnóstico , Adulto , Humanos , MasculinoRESUMEN
The effects of cocaine on the heart and peripheral circulation were examined in seven mongrel dogs. Hemodynamic variables, in addition to data on ventricular relaxation, mean circulatory filling pressure and arterial compliance, were measured during an intravenous infusion (0.5 mg/kg per min) of cocaine. Holter monitor recordings (6 h) and coronary arteriograms were also obtained. Cocaine increased (p less than 0.01) mean aortic pressure from 72 +/- 5 to 92 +/- 5, left ventricular systolic pressure from 102 +/- 3 to 121 +/- 5, left ventricular end-diastolic pressure from 4.9 +/- 1.3 to 8.2 +/- 1.4 and mean circulatory filling pressure from 7.9 +/- 0.4 to 10.9 +/- 0.5 mm Hg. Cardiac index and stroke volume decreased (p less than 0.01) from 166 +/- 17 to 125 +/- 8 ml/min per kg and from 44 +/- 4 to 29 +/- 3 ml, respectively. Ejection fraction decreased (p less than 0.01) from 61 +/- 1 to 49 +/- 3%. Heart rate, first derivative of left ventricular pressure (dP/dt) and right atrial, mean pulmonary artery and pulmonary artery wedge pressures did not change. The result was a 58% increase in systemic vascular resistance and a 32% decrease in arterial compliance. The pressure gradient for venous return did not change, but resistance to venous return increased 42%. Cocaine prolonged (p less than 0.05) the half-time of left ventricular isovolumic relaxation from 13.4 +/- 0.8 to 16.4 +/- 0.8 ms and the time constant of left ventricular isovolumic relaxation from 19.3 +/- 1.2 to 23.6 +/- 1.1 ms.(ABSTRACT TRUNCATED AT 250 WORDS)