RESUMEN
We aimed to evaluate efficacy and tolerability of a protocol including lifestyle modifications and a novel combination of dietary supplements in prehypertension. A prospective, double-blind, randomised, placebo-controlled trial was conducted in 176 subjects (103 men, aged 52±10 years), with blood pressure (BP) of 130-139 mm Hg systolic and/or 85-89 mm Hg diastolic entered. After a single-blind run-in period, participants were randomised to twice daily placebo (n=88) or a commercially available combination pill (n=88). Primary endpoints were the differences in clinic BP between the two groups at the end of the trial. Secondary endpoints included intragroup differences in clinic BP during the study period and response rates (that is, BP <130/85 mm Hg or a BP reduction >5 mm Hg on week 12). Baseline characteristics were similar among the treatment groups. At 12 weeks, the supplement group had lower systolic BP (124±9 versus 132±7 mm Hg, P<0.0001) and similar diastolic BP (81±8 versus 82±7 mm Hg, P=0.382) compared to the placebo group. With respect to baseline measures, changes in BP with supplements were statistically significant for systolic (-9.3±4.2 mm Hg, P<0.0001) and diastolic values (-4.2±3.6 mm Hg, P<0.0001). Changes versus baseline in systolic and diastolic BP, conversely, were not different on placebo. The overall response rate at week 12 was significantly greater with supplements than placebo (58% (51 of 88) and 25% (22 of 88), respectively, P<0.0001). This randomised trial shows that combination of supplements with BP-lowering effect is an effective additional treatment to conventional lifestyle modifications for a better control of systolic BP in prehypertension.
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Antihipertensivos/uso terapéutico , Presión Sanguínea/efectos de los fármacos , Suplementos Dietéticos , Prehipertensión/tratamiento farmacológico , Adulto , Antihipertensivos/efectos adversos , Suplementos Dietéticos/efectos adversos , Método Doble Ciego , Combinación de Medicamentos , Femenino , Humanos , Italia , Masculino , Persona de Mediana Edad , Prehipertensión/diagnóstico , Prehipertensión/fisiopatología , Estudios Prospectivos , Factores de Tiempo , Resultado del TratamientoRESUMEN
Noninvasive coronary angiography with multislice computed tomography (CT) scanners is feasible with high sensitivity and negative predictive value. The radiation exposure associated with this technique, however, is high and concerns in the widespread use of CT have arisen. We evaluated the diagnostic accuracy of coronary angiography using 320-row CT, which avoids exposure-intensive overscanning and overranging. We prospectively studied 118 unselected consecutive patients with suspected coronary artery disease (CAD) referred for invasive coronary angiography (ICA). All patients had 320-row CT within 1 week of ICA, which, together with quantitative analysis, served as the reference standard. Of the 65 out of 118 patients who were diagnosed as having CAD by ICA, 64 (98 %) were correctly identified at 320-row CT. Noteworthy, 320-row CT correctly detected CAD in 3 patients with atrial fibrillation and ruled out the disease in the other 8 patients. From 151 significant coronary stenoses detected on ICA, 137 (91 %) were correctly identified with 320-row CT. In the per-patient analysis, sensitivity and specificity of 320-row CT were 98 and 91 %, respectively. In the per-vessel analysis, sensitivity and specificity of 320-row CT were 93 and 95 %, respectively. In the per segment analysis, sensitivity and specificity of 320-row CT were 91 and 99 %, respectively. Diameter stenosis determined with the use of CT showed good correlation with ICA (P < 0.001, R = 0.81) without significant underestimation or overestimation (-3.1 ± 24.4 %; P = 0.08). Comparison of CT with ICA revealed a significantly smaller effective radiation dose (3.1 ± 2.3 vs. 6.5 ± 4.2 mSv; P < 0.05) and amount of contrast agent required (99 ± 51 vs. 65 ± 42 ml, P < 0.05) for 320 row CT. The present study in an unselected population including patients with atrial fibrillation demonstrates that 320-row CT may significantly reduce the radiation dose and amount of contrast agent required compared with ICA while maintaining a very high diagnostic accuracy.
Asunto(s)
Angiografía Coronaria/métodos , Enfermedad de la Arteria Coronaria/diagnóstico por imagen , Estenosis Coronaria/diagnóstico por imagen , Vasos Coronarios/diagnóstico por imagen , Tomografía Computarizada Multidetector , Anciano , Distribución de Chi-Cuadrado , Femenino , Humanos , Masculino , Persona de Mediana Edad , Variaciones Dependientes del Observador , Valor Predictivo de las Pruebas , Estudios Prospectivos , Dosis de Radiación , Reproducibilidad de los Resultados , Sensibilidad y Especificidad , Índice de Severidad de la EnfermedadRESUMEN
AIM: The aim of this study was to assess if knowing the interatrial conduction time is useful to better program atrioventricular delay in sequential pacing. The study proposes a new echo-Doppler method to measure interatrial conduction time, correlating it with electrophysiological measures. METHODS: The new method was tested in 30 subjects who underwent electrophysiological study. Interatrial conduction time by new method was taken during atrial pacing as the interval between the artefact of electrocardiogram pacing, shown on screen echo, and the onset of the A wave of the echo-Doppler mitral inflow. The electrophysiological measures were obtained, in the same subjects and at the same time, by a decapolar catheter in coronary sinus as intervals between the artefact of atrial pacing and the first positive left atrial deflection at proximal (C7C8) and distal (C1C2) electrodes. RESULTS: Echo-Doppler mean time was 114±12 ms, electrophysiological time was 107±14 ms at C7C8 and 124±11 ms at C1C2. Statistical analysis showed a good correlation (r=0.92, P<0.001) and accord (mean difference=6.6 ms) between the two methods. CONCLUSION: The new method to measure interatrial conduction time is consistent with the electrophysiological method; it could be particularly useful in programming the best AV delay in sequential and biventricular pacing, to avoid atrial contraction against a closed mitral valve.
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Función Atrial , Ecocardiografía Doppler , Técnicas Electrofisiológicas Cardíacas , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
BACKGROUND: Middle-aged women have a lower prevalence of coronary artery disease (CAD) compared with age-matched men, but mechanisms underlying this phenomenon remain controversial. To verify whether there is a link between circulating endothelial progenitor cells (EPCs) and gender-specific difference of CAD, we compared subpopulations of EPCs among postmenopausal normal women, patients with CAD, and age-matched men. METHODS: We studied 71 consecutive middle-aged patients with stable CAD (30 postmenopausal women and 41 men) and 40 middle-aged normal controls (20 postmenopausal women and 20 men). Blood samples were drawn at time of coronary angiography and subpopulations of EPCs were measured by flow cytometry. RESULTS: Women and men with CAD had similar age, risk factors, clinical presentation, left ventricular function, extension of CAD, and medical therapy at time of coronary angiography. Hematologic analysis showed that men and women with CAD had similar white cell count, mononuclear cells, and subpopulations of EPCs. Postmenopausal normal women, conversely, had significantly higher absolute numbers of CD34+, CD133+, CD105+ and CD14+ cells than other groups. CONCLUSIONS: Increased numbers of subpopulations of EPCs in normal postmenopausal women might contribute to the gender-specific difference of CAD in middle age. Lack of difference in EPCs between women and men with CAD suggests that stem cells become unable to play a protective role when the disease is clinically evident.
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Células Endoteliales/metabolismo , Posmenopausia/metabolismo , Células Madre/metabolismo , Antígeno AC133 , Antígenos CD/metabolismo , Estudios de Casos y Controles , Angiografía Coronaria , Enfermedad de la Arteria Coronaria/metabolismo , Endoglina , Femenino , Citometría de Flujo , Glicoproteínas/metabolismo , Humanos , Masculino , Persona de Mediana Edad , Péptidos/metabolismo , Receptores de Superficie Celular/metabolismoRESUMEN
BACKGROUND: C-reactive protein (CRP) induces adhesion molecule expression by endothelial cells. However, the effects of CRP on chemokine expression by endothelial cells are not known. METHODS AND RESULTS: We tested the effects of CRP on the production of the chemokines monocyte chemoattractant protein-1 (MCP-1) and RANTES in cultured human umbilical vein endothelial cells. The secretion of chemokines was assessed by ELISA. Incubation with 100 microgram/mL recombinant human CRP induced a 7-fold increase in MCP-1 but no change in RANTES secretion. We showed that the effect of CRP on MCP-1 was present even at 5 microgram/mL CRP, with stepwise increases as the CRP concentration was increased to 10, 50, and 100 microgram/mL. The effect of CRP on MCP-1 induction was not influenced by aspirin (at concentrations up to 1 mmol/L), but it was significantly inhibited by 5 micromol/L simvastatin. The peroxisome proliferator-activated receptor-alpha activators fenofibrate (100 micromol/L) and Wy-14649 (100 micromol/L) almost completely abolished the induction of MCP-1, but the peroxisome proliferator-activated receptor-gamma activator ciglitazone had only a moderate effect. CONCLUSIONS: These results further strengthen the role of CRP in the pathogenesis of vascular inflammation and, likely, atherosclerosis and provide a crucial insight into a novel mechanism of action of anti-atherosclerosis drugs such as simvastatin and fenofibrate.
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Proteína C-Reactiva/farmacología , Quimiocina CCL2/metabolismo , Endotelio Vascular/efectos de los fármacos , Hipolipemiantes/farmacología , Células Cultivadas , Quimiocina CCL5/metabolismo , Relación Dosis-Respuesta a Droga , Endotelio Vascular/citología , Endotelio Vascular/metabolismo , Fenofibrato/farmacología , Humanos , Receptores Citoplasmáticos y Nucleares/metabolismo , Simvastatina/farmacología , Factores de Tiempo , Factores de Transcripción/metabolismoRESUMEN
BACKGROUND: The acute-phase reactant C-reactive protein (CRP) is an important risk factor for coronary heart disease. However, the possible effects of CRP on vascular cells are not known. METHODS AND RESULTS: We tested the effects of CRP on expression of adhesion molecules in both human umbilical vein and coronary artery endothelial cells. Expression of vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM-1), and E-selectin was assessed by flow cytometry. Incubation with recombinant human CRP (10 microg/mL) for 24 hours induced an approximately 10-fold increase in expression of ICAM-1 and a significant expression of VCAM-1, whereas a 6-hour incubation induced significant E-selectin expression. Adhesion molecule induction was similar to that observed in endothelial cells activated with interleukin-1beta. In coronary artery endothelial cells, induction of ICAM-1 and VCAM-1 was already present at 5 microg/mL and reached a maximum at 50 microg/mL, at which point a substantial increase in expression of E-selectin was also evident. The CRP effect was dependent on presence of human serum in the culture medium, because no effect was seen in cells cultured with serum-free medium. In contrast, interleukin-1beta was able to induce adhesion molecule expression in the absence of human serum. CONCLUSIONS: CRP induces adhesion molecule expression in human endothelial cells in the presence of serum. These findings support the hypothesis that CRP may play a direct role in promoting the inflammatory component of atherosclerosis and present a potential target for the treatment of atherosclerosis.
Asunto(s)
Proteína C-Reactiva/metabolismo , Endotelio Vascular/metabolismo , Mediadores de Inflamación/metabolismo , Vasculitis/metabolismo , Arteriosclerosis/etiología , Arteriosclerosis/inmunología , Proteína C-Reactiva/inmunología , Proteína C-Reactiva/farmacología , Moléculas de Adhesión Celular/biosíntesis , Células Cultivadas , Vasos Coronarios , Medio de Cultivo Libre de Suero/farmacología , Selectina E/biosíntesis , Endotelio Vascular/citología , Endotelio Vascular/efectos de los fármacos , Citometría de Flujo , Humanos , Mediadores de Inflamación/inmunología , Mediadores de Inflamación/farmacología , Molécula 1 de Adhesión Intercelular/biosíntesis , Interleucina-1/metabolismo , Interleucina-1/farmacología , Proteínas Recombinantes/inmunología , Proteínas Recombinantes/metabolismo , Proteínas Recombinantes/farmacología , Venas Umbilicales , Molécula 1 de Adhesión Celular Vascular/biosíntesis , Vasculitis/etiologíaAsunto(s)
Arteriosclerosis/inmunología , Helicobacter pylori/inmunología , Imitación Molecular , Anciano , Anticuerpos Antibacterianos/efectos adversos , Anticuerpos Antibacterianos/inmunología , Antígenos , Antígenos Bacterianos/inmunología , Western Blotting , Arterias Carótidas/inmunología , Reacciones Cruzadas/inmunología , Femenino , Humanos , Sueros Inmunes/inmunología , Masculino , Persona de Mediana Edad , Peso MolecularRESUMEN
Helicobacter pylori is one of four organisms often investigated for ari association with ischaemic heart disease. The four, including Chlamydia pneumoniae, Cytomegalovirus and Herpes virus, cause low-grade, life-long infections that can produce a persistent inflammation, the kind that leads to heart disease. Several studies suggest an association, but others suggest none. Patients with poor access to medical care are more likely to become infected and also more likely to suffer from coronary artery disease. Although the literature data are provocative and interesting, the two things may not be related. Helicobacter pylori infection is quite prevalent among individuals without ischaemic heart disease and absent in many of those with ischaemic heart disease. Thus, more definite answers about whether there is any link between Helicobacter pylori and cardiovascular disease are needed. It would be essential to establish the specific mechanisms that possibly confer vulnerability or protection toward coronaropathy. But a definite answer could come from clinical trials designed to test whether antibiotics can prevent the disease. Until now, no randomised trial has suggested a positive effect of Helicobacter pylori eradication in reducing the incidence of cardiac events.
Asunto(s)
Infecciones por Helicobacter/microbiología , Helicobacter pylori/patogenicidad , Isquemia Miocárdica/microbiología , Salud Global , Infecciones por Helicobacter/epidemiología , Humanos , Incidencia , Isquemia Miocárdica/epidemiología , Prevalencia , Factores de RiesgoRESUMEN
BACKGROUND: Peroxisome proliferator-activated receptor-gamma (PPARgamma) is expressed in atherosclerotic plaques and in endothelial cells. The possible effects of PPARgamma activators on endothelial activation and inflammatory response within the plaque are currently unknown. METHODS AND RESULTS: We tested the hypothesis that PPARgamma activators inhibit vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecule (ICAM-1) expression in cultured endothelial cells (evaluated by flow cytometry) and homing of monocyte/macrophages to atherosclerotic plaques in vivo. In endothelial cells, the PPARgamma agonists troglitazone at 100 micromol/L and 15-deoxy-(Delta12,14)-prostaglandin J(2) (15d-PGJ2) at 20 micromol/L markedly attenuated the tumor necrosis factor-induced expression of VCAM-1 and ICAM-1. A significant inhibition of VCAM-1 expression was also evident at 5 and 10 micromol/L 15d-PGJ2 and 20 micromol/L troglitazone. Expression of E-selectin and PECAM-1 was not altered. To confirm the biological relevance of these results, we assessed the effects of troglitazone on monocyte/macrophage homing to atherosclerotic plaques in apoE-deficient mice. A 7-day treatment with troglitazone (400 mg/kg) significantly reduced monocyte/macrophage homing to atherosclerotic plaques (236+/-77 versus 177+/-43 macrophages, P=0.03); an even more striking inhibition was found at 3200 mg/kg troglitazone (344+/-76 versus 172+/-83 macrophages, P=0.005). CONCLUSIONS: PPARgamma activators inhibit expression of VCAM-1 and ICAM-1 in activated endothelial cells and significantly reduce monocyte/macrophage homing to atherosclerotic plaques. These findings suggest that PPARgamma activators, currently used in treatment of type II diabetes, may have beneficial effects in modulating inflammatory response in atherosclerosis.
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Arteriosclerosis/tratamiento farmacológico , Molécula 1 de Adhesión Intercelular/fisiología , Receptores Citoplasmáticos y Nucleares/efectos de los fármacos , Tiazolidinedionas , Factores de Transcripción/efectos de los fármacos , Molécula 1 de Adhesión Celular Vascular/fisiología , Vasculitis/tratamiento farmacológico , Animales , Movimiento Celular/efectos de los fármacos , Células Cultivadas , Cromanos/uso terapéutico , Endotelio Vascular/efectos de los fármacos , Humanos , Molécula 1 de Adhesión Intercelular/análisis , Macrófagos/efectos de los fármacos , Macrófagos/fisiología , Ratones , Monocitos/efectos de los fármacos , Monocitos/fisiología , Molécula-1 de Adhesión Celular Endotelial de Plaqueta/análisis , Tiazoles/uso terapéutico , Troglitazona , Molécula 1 de Adhesión Celular Vascular/análisisRESUMEN
The high frequency of premature atherosclerosis in patients with homocystinuria suggested the hypothesis of an association between hyperhomocysteinemia and coronary heart disease. Experimental studies have shown that severe homocysteinemia has toxic effects on the endothelium and may alter haemostatic balance. Although case controls studies have suggested a significant association between mild hyperhomocyst(e)inemia and coronary heart disease, prospective studies have not completely confirmed these findings. Results from the ongoing randomized trials will help determine whether reduction of homocysteine levels will be associated with a reduction of cardiac events and possibly mortality in patients.
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Enfermedad de la Arteria Coronaria/etiología , Homocisteína/metabolismo , Hiperhomocisteinemia/complicaciones , Animales , Estudios de Casos y Controles , Enfermedad de la Arteria Coronaria/epidemiología , Enfermedad de la Arteria Coronaria/metabolismo , Femenino , Humanos , Incidencia , Masculino , Estudios Prospectivos , Medición de Riesgo , Sensibilidad y EspecificidadRESUMEN
Syndrome X may be caused by a coronary microvascular dysfunction, possibly due to abnormalities in coronary endothelial function. Previous studies suggested that endothelin-1 (ET-1) might be involved in the pathogenesis of syndrome X. Baseline arterial and coronary sinus ET-1 levels were measured in 13 patients with syndrome X (10 women, 52+/-7 years) and in 8 control patients (5 women, 46+/-11 years). ET-1 was also measured after atrial pacing in 12 patients with syndrome X and all controls. To simultaneously assess the activity of nitric oxide, guanosine 3'-5'-cyclic monophosphate (cGMP) was also measured in 11 patients with syndrome X and 7 controls. Baseline arterial (2.27+/-0.46 vs. 1.90+/-0.22 pg/ml, p<0.05) and coronary sinus (2.03+/-0.43 vs. 1.68+/-0.28 pg/ml, p = 0.06) ET-1 plasma levels were higher in patients than in controls. After pacing, arterial ET-1 levels did not change in either group and coronary sinus ET-1 levels were also unchanged in controls. In contrast, coronary sinus ET-increased significantly in response to atrial pacing in patients with syndrome X (p = 0.023), and differences between coronary sinus ET-1 levels of patients with syndrome X and controls after pacing became highly significant (2.22+/-0.45 vs. 1.69+/-0.20 pg/ml, respectively, p = 0.006). No significant differences in arterial and coronary sinus cGMP concentrations were found between the 2 groups, both at baseline and after pacing. Our findings suggest that an increased vasoconstrictor activity of microvascular endothelium is present in at least some patients with syndrome X and may be involved in the pathogenesis of the syndrome.
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Estimulación Cardíaca Artificial , Endotelina-1/sangre , Angina Microvascular/sangre , Adulto , GMP Cíclico/sangre , Endotelio Vascular/fisiopatología , Femenino , Humanos , Masculino , Angina Microvascular/fisiopatología , Angina Microvascular/terapia , Persona de Mediana EdadRESUMEN
The effects of a beta blocker (atenolol), a calcium antagonist (amlodipine), and a nitrate (isosorbide-5-mononitrate) on anginal symptoms in 10 patients with syndrome X were assessed in a crossover, double-blind, randomized trial. Only atenolol was found to significantly improve chest pain episodes, suggesting that it should be the preferred drug when starting pharmacologic treatment of patients with syndrome X.
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Antagonistas Adrenérgicos beta/uso terapéutico , Amlodipino/uso terapéutico , Atenolol/uso terapéutico , Dinitrato de Isosorbide/uso terapéutico , Angina Microvascular/tratamiento farmacológico , Vasodilatadores/uso terapéutico , Análisis de Varianza , Estudios Cruzados , Método Doble Ciego , Femenino , Humanos , Persona de Mediana Edad , Estadísticas no Paramétricas , Resultado del TratamientoRESUMEN
Genotype analysis by using the p13E-11 probe and other 4q35 polymorphic markers was performed in 122 Italian facioscapulohumeral muscular dystrophy families and 230 normal controls. EcoRI-BlnI double digestion was routinely used to avoid the interference of small EcoRI fragments of 10qter origin that were found in 15% of the controls. An EcoRI fragment ranging between 10 and 28 kb that was resistant to BlnI digestion was detected in 114 of 122 families (93%) comprising 76 familial and 38 isolated cases. Among the unaffected individuals, 3 were somatic mosaics and 7, carrying an EcoRI fragment larger than 20 kb, could be rated as nonpenetrant gene carriers. In a cohort of 165 patients with facioscapulohumeral muscular dystrophy we found an inverse correlation between fragment size and clinical severity. A severe lower limb involvement was observed in 100% of patients with an EcoRI fragment size of 10 to 13 kb (1-2 KpnI repeats left), in 53% of patients with a fragment size of 16 to 20 kb (3-4 KpnI repeats left), and in 19% of patients with a fragment size larger than 21 kb (>4 KpnI repeats left). Our results confirm that the size of the fragment is a major factor in determining the facioscapulohumeral muscular dystrophy phenotype and that it has an impact on clinical prognosis and genetic counseling of the disease.
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Cromosomas Humanos Par 4/genética , Distrofias Musculares/genética , Adulto , Humanos , Distrofias Musculares/fisiopatología , Linaje , Fenotipo , Pronóstico , Factores de Riesgo , Secuencias Repetidas en TándemRESUMEN
BACKGROUND: There are limited data about the circadian distribution of ischemic episodes in patients with variant angina. Furthermore, no previous study investigated whether ischemia-related ventricular arrhythmias follow a circadian variation in these patients. METHODS: The circadian variation of transient ischemia and ischemia-induced ventricular arrhythmias was assessed by cosinor methodology on 24-hour Holter recordings of 26 patients with variant angina. RESULTS: On the whole, 301 ischemic episodes were detected in the population, with premature ventricular complexes occurring in 49 of them (16%). Ischemic episodes followed a typical circadian variation (acrophase hr 02:36, p < 0.01) in the total sample. However, a significant circadian variation of ischemic episodes was detectable in the 14 patients without (n = 167, acrophase hr 04:00, p < 0.0001), but not in the 12 patients with (n = 134, p = 0.14) hemodynamically significant coronary stenoses, independently of the location (anterior/inferior) of ischemia. There was no significant circadian variation of ischemia-related ventricular arrhythmias. CONCLUSIONS: Among patients with variant angina, a clearcut circadian variation of ischemia is present in those without, but not in those with, hemodynamically significant coronary artery stenoses, thus suggesting that different pathophysiologic mechanisms may operate, at least in part, in triggering coronary spasm in these two subgroups of patients. There was no significant circadian variation of ischemia-related ventricular arrhythmias in these patients.
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Angina Pectoris Variable/complicaciones , Isquemia Miocárdica/complicaciones , Angina Pectoris Variable/fisiopatología , Arritmias Cardíacas/etiología , Ritmo Circadiano , Humanos , Isquemia Miocárdica/fisiopatología , Disfunción Ventricular/complicaciones , Disfunción Ventricular/fisiopatologíaRESUMEN
A low heart rate variability (HRV) has been shown to be a powerful predictor of cardiac events in patients surviving an acute myocardial infarction (MI), but it is not clear yet which among the HRV parameters has the best predictive value. Time domain and frequency domain HRV was assessed on 24-hour predischarge Holter recording of 239 patients with a recent MI. Patients were followed up for 6 to 54 months (median 28), during which 26 deaths (11%) occurred, 19 of which were cardiac in origin and 12 were sudden. Most HRVs did not show any difference between patients with or without mortality end points, but the average low-frequency and low-frequency/high-frequency ratio was lower in patients with events. However, when dichotomized according to cut points that maximized the risk of sudden death, several HRVs were significantly predictive of clinical end points. Overall, the mean of the standard deviations of all RR intervals for all 5-minute segments and the standard deviation of the mean RR intervals for all 5-minute segments were the time domain variables most significantly associated with mortality end points, whereas very low frequency was the most predictive frequency domain variable. Compared with the best time domain variables, very low frequency showed a better sensitivity (0.27 to 0.42 vs 0.19 to 0.33) for end points with only a small loss in specificity (0.92 vs 0.96). On multivariate Cox proportional analysis, a left ventricular ejection fraction <40% and a number of ventricular premature beats > or = 10/hour were the most powerful independent predictors for all end points, whereas no HRV was independently associated with the events. A low frequency/high frequency ratio < 1.05 only had a borderline association with sudden death (RR = 2.86, p = 0.076). Our data show a strong association between HRV and mortality in patients surviving a recent MI, with a slight better sensitivity of frequency domain analysis. In our study, however, HRV did not add independent prognostic information to more classic prognostic variables (e.g., left ventricular function and ventricular arrhythmias).
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Frecuencia Cardíaca , Infarto del Miocardio/mortalidad , Anciano , Análisis de Varianza , Muerte Súbita Cardíaca , Electrocardiografía Ambulatoria , Femenino , Estudios de Seguimiento , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/fisiopatología , Valor Predictivo de las Pruebas , Pronóstico , Volumen SistólicoRESUMEN
OBJECTIVES: The aim of this study was to examine the prevalence of psychological distress and of its major determinants in acute coronary patients and in a control group. BACKGROUND: The prevalence and major determinants of psychological distress in acute coronary patients are not clear. METHODS: One hundred and thirty cardiac patients (110 men, age 56+/-9; 85 with acute myocardial infarction and 45 with unstable angina) and 102 controls hospitalized for acute trauma (70 men, age 55+/-9 years) were studied and the level of psychological distress estimated by a Modified Maastricht Questionnaire, self-ratings and ratings by a close relative. Major determinants of psychological distress were assessed by the Life Events Assessment, the Social Support Questionnaire and the Ways of Coping Checklist. RESULTS: The average level of psychological distress was significantly higher (p < 0.001) in coronary patients than in controls in all tests (self-evaluation=7.1+/-2.3 vs 4.3+/-2.4; relative-evaluation = 7.4+/-2.4 vs 4.2+/- 2.5; Modified Maastricht Questionnaire=91+/-32 vs 59+/-30). Cardiac patients reported significantly higher (p < 0.05) levels of social isolation (28.9+/-11.1 vs 23.4+/-8.8), self-blame (7.2+/-1.9 vs 5.8+/- 1.6) and avoidance (21.1+/-3.5 vs 18.9+/-3) and more painful life events (3.9+/-3.8 vs 2.6+/-2.2), than controls. However, not all patients had evidence of distress; indeed, cluster analysis identified a subgroup that comprised 75% of controls and 25% of cardiac patients with no determinants eliciting distress, while the other four subgroups, with one or more determinants of distress, comprised about 75% of patients and only 25% of controls. CONCLUSIONS: These results show that a high level of psychological distress is detectable in about 75% of patients with acute myocardial infarction or unstable angina and is related to one or more major determinants.
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Adaptación Psicológica , Angina Inestable/psicología , Infarto del Miocardio/psicología , Rol del Enfermo , Estrés Psicológico/complicaciones , Adulto , Anciano , Mecanismos de Defensa , Femenino , Humanos , Masculino , Persona de Mediana Edad , Inventario de Personalidad , Factores de RiesgoRESUMEN
BACKGROUND: Previous studies have reported an association between chronic Helicobacter pylori infection and ischemic heart disease. However, it is not clear whether this association is really due to the virulence of the bacterium or is merely the result of confounding factors (in particular, age and social class). METHODS AND RESULTS: We assessed the prevalence of infection by Helicobacter pylori and by strains bearing the cytotoxin-associated gene-A (CagA), a strong virulence factor, in 88 patients with ischemic heart disease (age, 57+/-8 years; 74 men) and in 88 age- and sex-matched controls (age, 57+/-8 years; 74 men) with similar social background. Prevalence of Helicobacter infection was significantly higher in patients than in controls (62% versus 40%; P=.004), with an odds ratio of 2.8 (95% CI, 1.3 to 7.4; P<.001) adjusted for age, sex, main cardiovascular risk factors, and social class. Patients with ischemic heart disease also had a higher prevalence of CagA-positive strains (43% versus 17%; P=.0002), with an adjusted odds ratio of 3.8 (95% CI, 1.6 to 9.1; P<.001). Conversely, prevalence of CagA-negative strains was similar in patients and controls (19% versus 23%), with an adjusted odds ratio of 0.8 (95% CI, 0.4 to 1.4). CONCLUSIONS: The association between Helicobacter pylori and ischemic heart disease seems to be due to a higher prevalence of more virulent Helicobacter strains in patients. These results support the hypothesis that Helicobacter pylori may influence atherogenesis through low-grade, persistent inflammatory stimulation.
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Antígenos Bacterianos , Infecciones por Helicobacter/complicaciones , Helicobacter pylori , Isquemia Miocárdica/etiología , Anciano , Proteínas Bacterianas/análisis , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
OBJECTIVES: We sought to investigate whether patients with syndrome X have an abnormal perception of cardiac pain. BACKGROUND: Previous studies have reported an increased sensitivity to potentially painful cardiac stimuli in patients with syndrome X. However, it is not clear whether this increase is due to an increased perception of pain or to an enhanced tendency to complain. METHODS: We assessed cardiac sensitivity to pain in 16 patients with syndrome X and 15 control subjects by performing right atrial and ventricular pacing with increasing stimulus intensity (1 to 10 mA) at a rate 5 to 10 beats higher than the patient's heart rate. False and true pacing were performed in random sequence, with both patients and investigators having no knowledge of the type of stimulation being administered. RESULTS: No control subject had pacing-induced pain; conversely, 8 patients with syndrome X reported angina during atrial pacing (50%, p < 0.01) and 15 during ventricular pacing (94%, p < 0.001). During atrial stimulation, both true and false pacing caused chest pain in a similar proportion of patients (50% vs. 63%, p = 0.61), whereas during ventricular stimulation, true pacing caused chest pain in a higher proportion of patients (94% vs. 50%, p < 0.05). Pain threshold and severity of pain (1 to 10 scale) were similar during true and false atrial pacing, whereas true ventricular pacing resulted in a lower pain threshold (mean +/- SD 3.7 +/- 3.0 vs. 7.9 +/- 2.8 mA, p < 0.001) and a higher level of pain severity (7.3 +/- 2.7 vs. 3.1 +/- 3.5, p < 0.001) than did false pacing. CONCLUSIONS: Patients with syndrome X frequently reported chest pain even in the absence of cardiac stimulation. Yet, in addition to this increased tendency to complain, they also exhibited a selective enhancement of ventricular painful sensitivity to electrical stimulation.