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INTRODUCTION AND OBJECTIVES: Calculation of cardiovascular risk in populations allows for developing and assessing of intervention programs and adapting health resources. While the Framingham System has been used in the past, a group of European researchers have proposed a different method called the Score project. The purpose of this paper is to compare the value of both methods for assessing cardiovascular risk. METHODS: In 6,775 evaluable hypertensive patients distributed over the 17 Spanish autonomous communities (ACs), the 10-year risk of experiencing a coronary event (CR) was calculated using the Framingham equation, while risk of coronary death (RCD) and vascular death (RVD) was calculated using the Score project system, both at baseline and after one year of blood pressure control with amlodipine at the required dose. A comparison was made of the capacity to detect risk differences by both methods between populations with known different risks, and in the same population as a result of blood pressure control. RESULTS: Both the Score and the Framingham systems detected the significant decrease in both CR and RCD or RVD at one year of application of the CORONARIA study protocol. Risk decrease measured by any of the two methods was significant (p < 0.05) overall, by genders, and by ACs. However, the Score System, unlike the Framingham system, could not detect the reported differences in the mortality risk for coronary and vascular disease between the ACs of the North and the South-East parts of Spain.

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Introducción y objetivos. El cálculo del riesgo cardiovascular en poblaciones permite desarrollar programas de intervención y adecuar recursos sanitarios. En el pasado se ha utilizado el sistema de Framingham, actualmente un grupo europeo ha propuesto el método Score. Nos proponemos comparar la utilidad de ambos métodos en la valoración del riesgo cardiovascular. Métodos. En 6.775 pacientes hipertensos valorables, procedentes de las 17 Comunidades Autónomas (CC.AA.) de España, se calculó el riesgo de padecer un accidente coronario (RC) en los siguientes 10 años (Framingham) y el riesgo de muerte por enfermedad coronaria (RMC) y por enfermedad vascular (RMV) (Score), tanto en situación basal como tras un año de control de la presión arterial mediante amlodipino. Se comparó la capacidad para detectar diferencias de riesgo entre distintas poblaciones con morbimortalidad cardiovascular diferente y en la misma población como consecuencia del control de la presión arterial. Resultados. Tanto el sistema Score como el de Framingham detectaron el descenso del riesgo de accidente coronario y del de muerte por causa coronaria o vascular, secundario al control de la presión arterial. El descenso del riesgo en cualquiera de los dos métodos fue significativo (p < 0,05) en datos globales, por sexos y por CC.AA. Sin embargo el sistema Score, al contrario que el de Framingham, no fue capaz de detectar las diferencias RMC y RMV, que han sido descritas entre las CC.AA. del norte de España y las del Sureste

Introduction and objectives. Calculation of cardiovascular risk in populations allows for developing and assessing of intervention programs and adapting health resources. While the Framingham System has been used in the past, a group of European researchers have proposed a different method called the Score project. The purpose of this paper is to compare the value of both methods for assessing cardiovascular risk. Methods. In 6,775 evaluable hypertensive patients distributed over the 17 Spanish autonomous communities (ACs), the 10-year risk of experiencing a coronary event (CR) was calculated using the Framingham equation, while risk of coronary death (RCD) and vascular death (RVD) was calculated using the Score project system, both at baseline and after one year of blood pressure control with amlodipine at the required dose. A comparison was made of the capacity to detect risk differences by both methods between populations with known different risks, and in the same population as a result of blood pressure control. Results. Both the Score and the Framingham systems detected the significant decrease in both CR and RCD or RVD at one year of application of the CORONARIA study protocol. Risk decrease measured by any of the two methods was significant (p < 0.05) overall, by genders, and by ACs. However, the Score System, unlike the Framingham system, could not detect the reported differences in the mortality risk for coronary and vascular disease between the ACs of the North and the South-East parts of Spain

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OBJECTIVES: Various articles describe the existence of differences in cardiovascular morbidity and mortality between different Spanish Autonomous Communities (SACs). We have intended to know if there are coherent differences in hypertensive patients cardiovascular risk. MATERIAL AND METHODS: 1,720 family physicians distributed in the 17 SACs as the number of inhabitants of each one selected 5 consecutive patients maximum within a period of 2 months, with blood pressure > or = 140/90 mmHg and at least another coronary risk factor. In 6,775 of 7,469 patients (51% males), the risk of a coronary event (CE) in the next 10 years according to Framingham equation and the risk of fatal cardiovascular event (RCV) according to Score formula were calculated. RESULTS: CE calculated in the group of patients in primary prevention (and without diabetes) in northern SACs (Cantábrico) was 18.8%, and 20.5% in south-east SACs (Mediterranean) (p < 0.0001). In addition, CE in secondary prevention was 26.1% in northern SACs and 28.6% in south-east SACs (p < 0.0001). The differences remained upon considering diabetics in primary prevention. There were no significant differences, however, in the risk of cardiovascular death (Score) between both areas, being 8.9% in the north and 8.8% in the south-east. CONCLUSIONS: Our study demonstrates that coronary risk is increased in hypertensive populations of south east SACs with respect to SACs of the north and to national average, while the risk of suffering a fatal cardiovascular event is not different.

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Objetivos. El objetivo del presente estudio fue evaluar la acción de la trimetazidina (TMZ), un fármaco antiisquémico, en el deterioro de la función sistólica que se produce en el miocardio sometido a isquemias breves y repetidas. Métodos. Se han analizado 12 perros mestizos de ambos sexos, randomizados a tratamiento con TMZ durante 7 días (grupo TMZ) o a tratamiento con placebo (grupo control). Se ha realizado un protocolo isquémico consistente en 20 obstrucciones completas de la arteria coronaria descendente anterior de 2 minutos de duración y separadas de 3 minutos de reperfusión entre ellas. Las variables analizadas al final de cada período de oclusión y reperfusión han sido: frecuencia cardíaca (FC), presión ventricular izquierda (PVI), dP/dt y las curvas de función regional de la zona isquémica y de una zona testigo (longitud telediastólica, telesistólica y fracción de acortamiento). Resultados. El grupo placebo está formado por 6 perros, con un peso medio de 30,08 kg; el grupo TMZ está constituido por 6 perros, con un peso medio de 24,25 kg. Los parámetros hemodinámicos (FC, PVI y dP/dt) no presentan diferencias significativas entre ambos grupos, con poca variabilidad de sus valores respecto a los basales en los diferentes procesos de isquemia/reperfusión. La fracción de acortamiento de la zona isquémica experimenta una caída, estadísticamente significativa, durante las sucesivas fases de isquemia en ambas series, alcanzando valores de acinesia/discinesia, con recuperación parcial durante las reperfusiones en el grupo placebo (aturdimiento), mientras que en la serie TMZ la recuperación es completa (64 por ciento frente 94 por ciento).Conclusiones. Nuestro estudio indica que la TMZ mejora la recuperación de la contractilidad miocárdica afectada por isquemias/reperfusiones breves y repetidas, limitando la aparición de miocardio aturdido (AU)

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n 1987 the results of the Consensus study were published, and showed that enalapril, an angiotensin convertor enzyme inhibitor (ACEI), was able to modify the clinical course of the heart failure syndrome thereby reducing mortality. Other ACEI later demonstrated the same effect on the different degrees of symptomatic heart failure, left ventricular dysfunction, myocardial infarction and more recently in diabetic patients. In 1996 studies on the betablockers carvedilol, bisoprolol and metoprolol showed their efficacy in reducing deaths due to progressive heart impairment and sudden death in chronic heart failure. The RALES study showed that small doses of spironolactone also improved the prognosis on this disease. Digital improves the quality of life but not the survival rate. Only amiodarone (among the antiarrhythmics) reduces sudden death. Other drugs and groups of drugs can not be considered for chronic outpatient treatment of heart failure. Multicenter trials make it possible to obtain scientific evidence for establishing rational treatments. Many groups of patients such as women, elderly people and the more severe cases of the disease are often not included in these trials. Occasionally, multicenter trials are badly designed (CIBIS and MCD), which in the case of betablockers, led to a substantial delay in their administration. Other times, as in the ELITE study, the results were badly interpreted. The knowledge obtained from these studies is slow in reaching patients, with few patients taking betablockers. It is known that most patients do not take the doses found to be effective in multicenter trials.

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INTRODUCTION AND OBJECTIVES: Hearts exposed to reversible ischemia stand a subsequent prolonged episode of coronary artery occlusion (ischemic preconditioning) better. The reduction of infarct size by means of preconditioning has been amply demonstrated, but the relationship between preconditioning and contractile function remains less well defined. In this study we assess the effect of a later ischemia on the regional contractility in a stunned-preconditioned myocardium. METHODS: We analyze the shortening fraction in the ischemic (dependent on the left anterior descending coronary artery), periischemic and control zone (dependent on the left circumflex coronary artery), using chronic implants of ultrasonic crystals in 17 adult mongrel dogs. In the control series, we quantified the effects of partial (30-60% reduction of coronary flow from the basal) and transitory (15 minutes) ischemic episode in the regional myocardial function in a "virgin" myocardium. In two other series, the myocardium was previously stunned-preconditioned through brief and repeated ischemias. Afterwards, at 5th day (series B) and at 15th day (series C), the dogs were subjected to ischemic episode similar to control ones. RESULTS: After comparing the results with the control series, we observed that the shortening fraction of the ischemic zone was decreased by 107% (p < 0.01) during partial ischemic episode when it was induced on the 5th day of the stunning-preconditioning (series B). CONCLUSIONS: In dogs, the brief and repeated episodes of ischemia could condition the contractile function so that a later partial and transitory reduction of coronary flow could induce a severe affectation of contractility expressed as a diskinetic area.

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INTRODUCTION AND OBJECTIVES: In previous studies we have observed ischemic processes of very brief duration (2 minutes) and with brief reperfusion (3 minutes), which have been repeated 20 times (ischemic protocol [IP]). They are capable of producing contractile dysfunction of the ischemic zone, with a decrease of 28.6% at 24 hours, and coronary blood flow maintenance (stunning). METHODS: The aim of this study is to examine the evolution of this dysfunction. The IP designed in our laboratory was used on 24 adult mongrel dogs. We measured regional myocardial function using a pair of implanted chronic ultrasonic crystals in the ischemic area (depending on the left anterior descending coronary artery) and a second pair in the control zone (depending on the left circumflex coronary artery). RESULTS: After analyzing results, we found that the shortening fraction decreased to 28.6% (p < 0.05) in 24 hours. During the subsequent five days the shortening fraction decreased to a minimum of 67.88% (p < 0.01), after which there was a progressive recovery that reached 18.95% (NS) below the base-line on the tenth day. We did not observe any significant variation in the hemodynamic parameters at any time. CONCLUSIONS: The repeated, very brief episodes of ischemia (in the experimental terms that we have explained) produced a contractile dysfunction which reached its maximum on the fifth day, and returned to normal on the tenth day. We hypothesize that these alterations could explain the episodes of left ventricular failure with spontaneous recuperation observed in stable myocardial ischemia, and for which no immediate cause has been found.

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INTRODUCTION AND OBJECTIVES: Myocardial ATP is produced mainly by fatty acid oxidation, a process in which the fatty acid metabolite carrier carnitine is needed to carry the metabolites into the mitochondria. Cardiac ischemia is associated with carnitine depletion. Our objective was to study the functional effect of L-carnitine on myocardium stunned by very brief, repeated ischemias, and to examine its actions in the recovery period. METHODS: The two series studied were the control series (7 dogs) and the carnitine series (7 dogs). L-carnitine was administered to the carnitine series at doses of 250 mg/kg/day starting 7 days before the ischemic protocol and continuing during the follow-up period (10 and 15 days). The ischemic protocol consisted of 20 anterior descending coronary artery occlusions lasting 2 min and with 3 min of reperfusion between occlusions. Global and regional cardiac function parameters were recorded daily. RESULTS: No differences in the global functional (haemodynamic) or ECG of the two series were found, but there were differences in regional myocardial function. The control series segment shortening fraction fell to dyskinesis values during the occlusion periods, then recovered during reperfusions. The segment shortening fraction worsened during the stunning period, reaching its maximal impairment on the 5th day, after which it returned to basal values on the 15th day. The carnitine series showed the same performance in the occlusion/reperfusion period. However, during the stunning period the segment shortening fraction recovered and reached values close to the basal ones maintained them during the follow-up period. CONCLUSIONS: L-carnitine induces an almost immediate recovery of myocardial contractility, when it has been affected by very brief, repeated coronary occlusions. It limits the myocardial stunning apparition.

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BACKGROUND: Smoking has been related to coronary heart disease, and, in men, to sudden death. The results of a case-control study designed to assess the relationship between smoking and all causes of sudden and premature death are reported. METHODS: A questionnaire on the previous history and causes of death of all people buried in the Municipal Cemetery of Valencia (1986-1987) was administered to the relatives of the deceased. Among 4718 deaths, 284 victims of sudden death were identified, and 495 people who had not died suddenly were randomly sampled as controls. RESULTS: The proportion of smokers among the women studied was extremely low in contrast to 58.9% of men in the sudden death study group and 59.2% of men in the non-sudden death study group who smoked. Smokers died on average 10 years younger than non-smokers in the sudden-death group (63.3 +/- 12.3 and 73.3 +/- 11.0 years respectively; P < 0.001), and 8 years earlier in the non-sudden death group (68.5 +/- 13.3 and 76.8 +/- 13.2 years, respectively; P < 0.001). A logistic regression model showed that smokers had an adjusted relative risk of 0.81 for sudden death compared with non-smokers (95% confidence interval [CI]: 0.45-1.46). Smokers 65 years of age or under had a 2.7 times greater risk (95% CI: 1.49-5.04) of premature death than non-smokers. Similar results were found in patients from the coronary- and cardiac-death subgroups. CONCLUSIONS: Smoking is an independent risk factor for premature death but not for sudden death.

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Ventricular extrasystoles and the complex forms of non-malignant ventricular arrhythmias clearly increase in the presence of left ventricular hypertrophy. Left ventricular hypertrophy constitutes a clear sudden death risk factor. The connection between possible malignant arrhythmias, which have also been reported in LVH patients, and an increased incidence of sudden death has not been established. Hypertension, electrical changes in the hypertrophic myocyte, the growth of the collagen matrix and ischaemia (even in the absence of macro-angiographic injuries) are factors present in this group of patients that contribute to the appearance of arrhythmias. The arrhythmogenic substrate of LVH has to do with reentry mechanisms due to fibrillar stretching and anisotropy, as well as with self-sustaining activity triggered by after-potentials that depend on activation of slow calcium channels.

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The aim of this paper is to analyze the behaviour of the muscular arteries during ventricular tachycardia in normal and in ischemic hearts. In 19/30 anaesthetized dogs in which a resistance vessel (gracilis muscle artery) was isolated (while innervation and venous backflow remained intact), we performed transient (20 min) coronary artery occlusions and ventricular overdriving (30 sec). A systolic left ventricular pressure decrease (144.2 +/- 18.2 mmHg vs 114 +/- 16.1) (p < 0.001) was produced with the coronary circumflex obstruction. Changes in the end-diastolic left ventricular pressure and muscular artery pressure were not significant. A new systolic left ventricular pressure decrease (114 +/- 16.1 mmHg vs 64.8 +/- 27) (p < 0.001) was induced when the ventricular overdriving (272.2 +/- 46.1 bpm) was added to the coronary circumflex obstruction. The end-diastolic left ventricular pressure increased (6.8 +/- 10.1 mmHg vs 18.3 +/- 4.8) (p < 0.001) and the muscular artery pressure increased (121 +/- 27.3 mmHg vs 158.1 +/- 21.3) (p < 0.01) in these circumstances. When the ventricular overdriving (275 +/- 70.7 bpm) was added to the left descendent anterior coronary occlusion a significative decrease of left systolic ventricular pressure (141 +/- 23 mmHg vs 84.4 +/- 28.4) (p < 0.01) and an increase of the muscular artery pressure (124.3 +/- 25 mmHg vs 149 +/- 25.1) (p < 0.01) was produced. Ventricular overdriving-induced hypotension produced an isolated muscular artery response with clear vasoconstrictor predominance, which indicates that there is a natural compensatory capacity with predominance of efferent sympathetic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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UNLABELLED: The aim of this work is to analyze the vascular tone behaviour of the muscular arteries in relation to the reflexes generated during aortic root obstruction when spontaneous heart rate is permitted and also with induced tachycardia. An experimental model used involved anaesthetized and intubated dogs in which a resistance vessel (gracilis muscle artery) was isolated, while innervation and venous backflow remained intact. Moderate (54.4 +/- 23.2 mmHg of mean increase in left ventricular pressure) and severe (240.1 +/- 92.5 mmHg) aortic obstructions for 30 s were provoked during spontaneous heart rate (n = 15) and during ventricular overdriving (n = 13) at 200, 250 and 300 bpm for 30 s. Ventricular overdriving at 200, 250, 300 and 400 bpm for 30 s without aortic root obstruction was induced in 20 dogs. Ventricular overdriving in intact hearts produced an initial decrease in the isolated muscular artery pressure of 12.0 +/- 7.2 mmHg (p < 0.01), 9.5 +/- 5.7 mmHg (p < 0.001), 13.6 +/- 8.6 mmHg (p < 0.001) and 14.3 +/- 8.7 mmHg (p < 0.01) at 200, 250, 300 and 400 bpm respectively followed by a recovery, so that at the end of overdriving (30 s), exceeded basal values in 11.9 +/- 10.0 mmHg (p < 0.05), 21.1 +/- 12.4 mmHg (p < 0.001), 21.9 +/- 10.4 mmHg (p < 0.001) and 36.1 +/- 21.3 mmHg (p < 0.001) for each overdriving rate respectively. Aortic obstruction during spontaneous heart rate produced and initial decrease in the isolated muscular artery pressure of 12.0 +/- 7.3 mmHg (p < 0.01), when the aortic obstruction were moderate, and 31.4 +/- 15.7 mmHg (p < 0.01) when the obstructions were severe, followed by a recovery of its basal values at the end of the obstruction time. Ventricular overdriving with aortic root obstruction did not produced significant changes in the isolated muscular artery pressure except in the highest rates of overdriving, that produced an increase of isolated muscular artery pressure of 23.9 +/- 16.2 mmHg (p < 0.01). IN CONCLUSION: ventricular overdriving-induced hypotension in intact hearts produces an isolated muscular artery response with clear vasoconstrictor predominance. Aortic obstruction-induced hypotension does not produce a vasoconstrictor response in the isolated muscular artery but rather an initial vasodilation response which does not revert to vasoconstriction at any point during the hypotensive process. Overdriving was not capable of inducing a peripheral vasoconstriction in presence of aortic root obstruction except in the highest rates of overdriving.

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