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The article discusses the status and management of heart failure disease in Spain. It states that the Spanish Society of Cardiology issued guidelines on how to manage heart failure in the country. In addition, heart failure is the main cause of hospitalization in older Spanish population. Moreover, drugs for heart failure management may be underused and there were scarcity of the care facilities for older patients.

Background: The alteration of contractile function after tachyarrhythmia ceases is influenced by the type of prior ischemia (acute coronary syndrome or ischemia inherent in a coronary revascularization procedure). We aimed to analyze cardiac dysfunction in an acute experimental model of supraphysiological heart rate preceded by different durations and types of ischemia., Material and Methods: Twenty-four pigs were included in: (S1) series of ventricular pacing; (S2, A and B) series with 10 or 20 min, respectively, of coronary occlusion previous to ventricular pacing; S3 with 20 brief, repeated ischemia/reperfusion processes prior to ventricular pacing and; (S4) control series. Overall cardiac function parameters and regional myocardial contractility at the apex and base of the left ventricle were recorded, as were oxidative stress markers (glutathione and lipid peroxide serum levels). Left ventricular pacing at 60% over baseline heart rate was performed for 2 h followed by 1 h of recovery., Results: High ventricular pacing rates preceded by short, repeated periods of coronary ischemia/reperfusion resulted in worse impairment of overall cardiac and regional function that continued to be altered 1 h after tachycardia ceased. There was significant reduction of stroke volume (26.9 ± 5.3 basal vs. 16 ± 6.2 ml; p<0.05), LVP; dP/dt and LAD flow (13.1 ± 1.5 basal vs. 8.4 ± 1.6 ml/min; p<0.05); the base contractility remained altered when recovering compared to baseline (base SF: 5.6 ± 2.8 vs. 2.2 ± 0.7%; p<0.05); and LPO levels were higher than less aggressive series at the end of recovery., Conclusions: Ischemia and tachycardia accumulate their effects, with increased cardiac involvement depending on the type of ischemia.

Background: High-rate short-duration ventricular pacing induces myocardial hypokinesis that persists once the hemodynamic conditions have been recovered. The aim was to study the factors that determine the persistence of myocardial dysfunction when ventricular tachycardia has ceased and hemodynamic conditions have been restored., Material/methods: An in vivo experimental pig model was used consisting of a ventricular pacing series (n=10), a ventricular pacing and aldosterone blockade (eplerenon) series (n=6), and a control series without ventricular pacing (n=6). Electrical stimulation was performed from the epicardial base of the left ventricle at a frequency 60% above the basal rate for 2 hours followed by a recovery period of 60 minutes. Cardiac and myocardial function parameters were studied. Plasma levels of aldosterone, renin activity, and glutathione were measured., Results: Electrically induced tachycardia produced hemodynamic and myocardial changes that persisted after stimulation had ceased, accompanied by an increase in aldosterone and a coronary flow decrease. These changes were not seen when aldosterone activity was blocked by eplerenon. There was a non-significant elevation in glutathione levels., Conclusions: These data show that although participation of other neurohormones cannot be ruled out, aldosterone blockade (eplerenon) ameliorates myocardial dysfunction persisting after ventricular tachycardia by preventing coronary endothelial dysfunction.

Background and Objective: Obesity is a major and independent cardiovascular risk factor. The aim of this study was to know overweight and obesity distribution in a sample of Spanish high systemic pressure patients (CORONARIA study), the risk factors associated and the calculated cardiovascular risk (CR) that the overweight produces., Material and Method: 1,720 family physicians included 7,087 hypertensive patients with at least another CR factor associated. Patients were classified depending on their body mass index: its value was < 25 kg/m2 in 1,150 patients; > or = 25 and < 30 kg/m2 in 3,724 (overweight); and > or = 30 kg/m2 in 2,213 patients (obesity)., Results: 83.7% of patients showed overweight or obesity; and 36.1% of women included were obese. Overweight was significantly more prevalent in the hypertensive population of Andalucía, Murcia, Canarias and Extremadura, and less frequent than the Spanish mean in Catalonia and Asturias. Hypertensive and obese patients showed higher prevalence of diabetes than normal weight patients (34.3% vs 24%); higher levels of triglycerides; high values of systemic pressure; and lower levels of high density lipoproteins-cholesterol; all these facts raised the CR, calculated value between a 19.7% in the overweight cases and a 11.6% in the obese patients compared with normal weight patients. Heart failure was two times more prevalent in obese patients., Conclusions: Overweight in hypertensive patients raises the cardiovascular risk by 20%, and has a strong association with diabetes and heart failure.

Introduction and Objectives: The presence of renal disease significantly alters the cardiovascular risk of patients with high blood pressure. However, few studies have examined renal parameters in primary care patients. The objectives of this study were to investigate cardiovascular risk and the factors influencing it in hypertensive patients with renal disease and to compare the findings with those in hypertensive patients without renal disease., Methods: The CORONARIA study involved primary care patients with hypertension from all regions of Spain and included two groups with different degrees of renal disease., Results: In total, 703 patients (9.8%) had renal disease. Hypertensive patients with renal disease had a worse cardiovascular risk profile than other hypertensives. The prevalence of diabetes was double in patients with renal disease. Moreover, the risk of a coronary event was significantly higher in those with renal disease. One-third of hypertensives with renal disease had another previously diagnosed cardiovascular disease. In addition, they more frequently had a history of angina, were twice as likely to have had a myocardial infarction, and were more than twice as likely to have undergone revascularization or to have peripheral vascular disease or cerebrovascular disease. Heart failure was four times more frequent in these patients with renal disease than in other hypertensives., Conclusions: Patients with hypertension and renal disease have a higher risk of cardiovascular disease, exhibit an increased prevalence of diabetes, and suffer from more extensive target organ damage.

Background and Objective: Diabetes mellitus is a prevalent disease with high cardiovascular mortality. Treatment of risk factors can reduce the associated cardiovascular risk. The CORONARIA study included 7253 patients with high risk systemic hypertension from different regions of Spain. The aim of this study was to analyze the cardiovascular risk (CR) of diabetic patients at baseline and after one-year follow-up., Patients and Method: A total of 2105 (29%) patients with type 2 diabetes and systemic hypertension are included in the CORONARIA study. The CR profile is evaluated at baseline and after treatment of systemic hypertension with amlodipine (5-10 mg), while other cardiovascular risk factors were also treated. Data were compared with non diabetics., Results: Patients with systemic hypertension in Spain show a very high prevalence of diabetes (29%); it is higher in women than men (p<0.05) and higher in secondary prevention than primary prevention (p<0.05). Prevalence diabetes was higher in Murcia, Andalucía, Extremadura and Comunidad Valenciana, and lower in Madrid and País Vasco than the Spanish mean. The CR in primary prevention was significantly higher in diabetics than in non-diabetics (female: 22.9% vs 12.3% in Framingham, and 10.1% vs 5.2% in REGICOR; male: 39.9% vs 27.8% in Framingham and 15.7% vs 10.3% in REGICOR). After one year treatment, cardiovascular risk decreased significantly in both groups of patients, but it did more in diabetics (Framingham: -11.6% vs -6.7%; REGICOR: -5.3% vs -2.8%)., Conclusions: Most patients with diabetes and systemic hypertension did not have an adequate control of CR factors and presented a high cardiovascular risk. Treatment reduced the CR significantly in a greater proportion of diabetic than non diabetic-patients.

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.

Background: The aim was to assess the effect of trimetazidine (TMZ) on mitochondrial alterations induced in a canine model of brief, repeated episodes of ischemia., Material/methods: Twelve crossbred dogs were analyzed, after double-blind randomization, to a 7-day treatment with either TMZ or placebo. Twenty brief, complete occlusions of the left anterior descending coronary artery were performed. Mitochondrial analysis entailed a qualitative (percentage of mitochondrial damage, merging, pairing, vacuoles, and lipofucsin granules) and a quantitative size analysis (major and minor axes, perimeter, and area) of the mitochondria in the ischemic and control zones., Results: Comparative study of the control zones revealed an increase in lipofucsin granules in the TMZ series and a greater percentage of damaged mitochondria and vacuoles. The control-zone mitochondria treated with TMZ presented a significant increase in the perimeter and major axis and a decrease in the minor axis (p<0.005). No significant differences were found between the series in the qualitative analysis of mitochondrial damage in the ischemic zone. The mitochondria in the TMZ series presented a greater major axis and perimeter than those in the placebo series (p<0.05), which presented a smaller minor axis., Conclusions: TMZ made the mitochondria adopt an elongated, "rod-like" morphology in both the control and ischemic zones. This is interpreted as an increase in the membrane surface. In the non-ischemic zone, TMZ produced an increase in mitochondrial turnover. There were no differences in the myocardium subjected to ischemia in both series in terms of observable mitochondrial damage.

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.

Objective: Evaluation of the effect of amlodipine on the hospitalizations for cardiovascular events (CVE) and their associated costs in patients with ischemic cardiopathy., Methods: Data from the multicenter, randomized, double-blind, placebo-controlled PREVENT (Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial) clinical trial were utilized. A tree-type model of decision was used in order to analyze the incremental costs expected from the treatment with amlodipine with regard to placebo. Hospitalization costs were estimated with regard to the DRG weights of the American Medicare adapted for the costs of average stay available in our environment., Results: Amlodipine reduced significantly the incidence of CVE that required hospitalization in contrast to placebo; 0.60 +/- 1.16 versus 0.77 +/- 1.31 (average +/- SD), p < 0.05. The expected direct expenses due to hospitalizations were higher in the placebo group than in the amlodipine group (saving of 205.76 Euro/patient). Total cost for patient in the amlodipine group was 1,723.52 Euro while in the placebo group was 1,929.28 Euro. When the relation cost/price shifted in the sensitivity analysis from 1.20 to 0.66 (cost of every hospitalization ranged between + 20% and -34%), the saving fluctuated from 330.56 Euro to 0. Accordingly, the breakeven point of the cost/price relation it is 0.66, and above this the treatment with amlodipine still generates savings in regard to its cost., Conclusions: Amlodipine is cost-effective in the treatment of the patients with ischemic cardiopathy, being able to reduce the hospital costs related to ischemic episodes in this type of patients.

Introduction: The diagnosis of chronic heart failure (CHF) is based on demonstrating the cardiac origin of clinical manifestations. Echocardiography is the method of choice for the detection of left ventricular systolic dysfunction (LVSD). Brain natriuretic peptide (BNP) rises during LVSD., Objectives: To analyze the plasma concentration of N-terminal brain natriuretic propeptide (NTproBNP) in a general adult population in relation to different spontaneous circumstances and to study its capacity for identifying patients with LVSD.Methods. A cardiological examination was made and plasma NTproBNP levels were measured in a randomized group of 203 people (49-81 years old) from the Community of Valencia., Results: The average NTproBNP concentration was 52.2 98.2 pmol/l. NTproBNP levels varied with age, gender and functional stage (NYHA). The highest NTproBNP values were observed in people who had previously suffered from acute pulmonary edema or who had an ejection fraction (EF) of less than 40%. There was also a significant elevation in patients with nocturnal dyspnea, orthopnea, atrial fibrillation, EF < or = 50%, angina, and ankle edema. The best concentration of NTproBNP for differentiating EF < or = 50% was 37.7 pmol/l, with 92% sensitivity and 68% specificity., Conclusions: The elevation of NTproBNP concentration indicates the cardiac origin of clinical manifestations and serves to select patients for echocardiographic examination. Low NTproBNP concentrations help to rule out LVSD.

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.

Stable angina pectoris is the most common clinical manifestation of chronic ischemic heart disease, the prognosis of which depends on many factors. The authors have analyzed the incidence, evolution and prognosis of this problem in Spain and have reviewed the methods to determine the diagnosis and degree of clinical severity. A careful clinical history, an electrocardiogram, and the evaluation of the severity of the ischemia and left ventricle systolic function are, in most cases, useful to determine the degree of disease severity and establish the prognosis. In other cases, more sophisticated or complex diagnostic techniques such as perfusion tests, stress echocardiography and lastly coronary arteriography, which is the only method currently available to study coronary anatomy are required to carry out an adequate study of the patient. At present, the therapeutic arsenal for the treatment of ischemic coronary disease is extensive, from both a pharmacological and revascularization point of view. Nonetheless it is essential to carry out aggressive therapy to control the risk factors. The decision as to the type of treatment required mainly depends on the severity of the ischemia and in the case of revascularization, on the clinical and anatomical factors as well as on the preferences of the patient and the experience and results of the medical-surgical group involved in the therapy of these patients.

This article presents the program for training in cardiology. The document was elaborated by the National Committee of the Specialty of Cardiology, from the Ministry of Health and Ministry of Education, and describes the theoretical and practical aspects of training in cardiology prevailing at present in Spain.

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.

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.

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.

Introduction: Our study was designed with the primary objective of evaluating the cardiac, overall and sudden mortality in patients with class IV heart failure (NYHA) managed with standard treatment and captopril (50 mg/8 hr. max.)., Material and Methods: 95 consecutive patients were enrolled in 21 hospitals and were followed for 6 months in order to design an interventional clinical trial to reduce sudden death., Results: Death occurred in 14 patients (14.7%; i.c. 8.3% - 23.5%; p < 0.05). There were no non-cardiovascular deaths in the group. There were 6 sudden death cases (42.9%; i.c. 16.9% - 68.8%, p < 0.05). Patients who died had a higher baseline end-diastolic (p < 0.05) and end-systolic (p < 0.01) diameter of the left ventricle (LV) and lower values of systolic (p < 0.01) and diastolic (p < 0.05) blood pressure. During the follow-up phase, heart rate, ventricular premature contraction, blood pressure and LV diameters decreased significantly in the whole group (p < 0.05, p < 0.001). We found no any differences during the follow-up phase between the patients who died and those who survived. In the patients who died we found no any differences between sudden death cases and the other death cases., Conclusions: Sudden death was less frequent than we had expected and due to this fact it is impossible for us to design an interventional trial.

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as "compensators", which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these system, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatments for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as "compensators", which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these systems, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at the cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatments for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.

Objective: To analyze whether nitroglycerin and nifedipine can reduce myocardial stunning due to very brief, repeated coronary ischemias., Material and Methods: In 33 anaesthetized and open chest dogs, the lengthening and shortening fractions were analyzed with ultrasonic crystals in the ischemic and control myocardial areas. Twenty repeated coronary occlusions of 2 minutes each, with a recovery time of 3 minutes between each occlusion, were induced. At the beginning of the experiment, nitroglycerin (0.3 mg i.v. and 80 micrograms/kg/min perfusion) was administered in series A (n = 8), nifedipine (5 mu/kg i.v. and 1 microgram/kg/min perfusion) in series B (n = 9). The results were compared with control results (n = 16) without drugs., Results: Changes in the shortening fraction of the ischemic area during coronary occlusions were similar in all three series; after the last occlusion the shortening fraction in the control series was -14.9% with respect to basal values, -14.6% in series A and -16.6% in series B. Sixty minutes after the last ischemia, the shortening fraction impairment in respect to the basal values was larger in the control series (-18.9%) and in series A (-16.9%). In series B there was recovery (-13.5%) (p < 0.05 vs control series)., Conclusions: Our study indicates that nitroglycerin does not seem to have cardioprotective effects against brief, repeated ischemia. However, nifedipine decreases postischemic dysfunction due to this model of ischemia, probably by avoiding the intracellular Ca overload produced during cardiac ischemia.

Recently the European Societies of Cardiology Atherosclerosis and Hypertension have published a document of Recommendations on the Prevention of Coronary Disease in Clinical Practice. The information given in the document has proven that a reduction in cholesterol reduces the risk of the onset of new coronary as well as cardiovascular mortality. It has been accepted that such reduction can induce the regression of the atheroma plaque, and the slowing of its progression. In Spain cardiovascular mortality has progressively decreased since 1975. This is true for the coronary caused mortality and the secondary to a cerebrovascular disease, the latter being that where the greatest change has been noticed, as well as in women. Probably, this trend may be explained by a better control on hypertension, as well as by a more adequate hospital net. Spain has one of the lowest rates of mortality due to coronary disease among the industrialized countries. Nevertheless, the cardiovascular mortality is still the first cause of death in Spain. Spanish cardiologist are convinced that the relationship between the levels of cholesterol and coronary risk happened in Spain, in quantitative terms, differently than in Central Europe and the USA. They consider that the "Mediterranean diet" is the protective factor.

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.

A total of 127 patients with different forms of obstruction to left ventricular outflow are studied. There were eight cases with supravalvular aortic stenosis, 79 with valvular aortic stenosis, 25 with hypertrophic subaortic stenosis, and 15 with subvalvular aortic stenosis. Clinical findings and electrocardiographic, radiographic, and angiohemodynamic data corresponding to these groups are reported, as well as the differential characteristics for each category from a clinical, electrocardiographic and radiographic point of view. The presence of a typical face, asymmetrical carotid and brachial pulses, absence of aortic ejection click and little or no aortic button on the chest roentgenogram reveals a supravalvular aortic stenosis. Valvular aortic stenosis shows aortic ejection click, poststenotic dilation of the ascending aorta, electrocardiographic signs of left ventricular hypertrophy and associated aortic regurgitation. Hypertrophic subaortic stenosis is characterized by a typical arterial pulse, marked "a" wave in the jugular venous pulse, double apical impulse on palpation and appearance or modification of the systolic ejection sound with Valsalva's maneuver.

Insufficiency on the tricuspid valve alone due to cardioarticular rheumatism is a rare condition. A 12-year-old boy had had six episodes of rheumatic fever over the previous 5 years. The only damage done to the heart was insufficiency of the tricuspid valve; none of the other valves were affected. The phonocardiographic response to the amyl nitrate and methoxamine tests as well as the correct evaluation of the jugular phlebogram confirmed the diagnosis of this valve pathology. The study of this heart condition was completed with the diagnosis of rheumatic fever (Jones' criteria, modified) and an angiohemodynamic evaluation of the patient (which must include left and right ventriculography using a Bourassa catheter on the right). This pathology is extremely rare and we have found no reference to it in the literature in this country.

Three hundred hospital patients with syncope (193 males and 107 females, mean age 61 +/- 17 years) were prospectively evaluated with a standard protocol. Associated diseases were found in 76.7% of cases. The incidence of heart diseases was 50.8% in males vs 32.7% in females (p less than 0.003). The cause of syncope was diagnosed in 250 patients (84%). The diagnosis was made at initial evaluation in 101 patients (group A); in the remaining patients (group B), no diagnosis was made in 25% (16.6% of the overall series) despite a wide array of investigations. Syncope due to arrhythmia was diagnosed in 57.6% (group A: 91.1% group B: 40.7; p less than 0.0001); cardiac syncope not due to arrhythmia was diagnosed in 4%, and other types of syncope in 21.6% (group A; 6.9%; group B: 29.1%; p less than 0.0001). It is concluded that a) the hospital population of patients with syncope represents a subgroup of advanced age and a high incidence of associated diseases; b) one third of patients were diagnosed at the initial evaluation, whereas in 25% of the remaining ones no diagnosis was obtained, and c) in these patients, arrhythmia is the most likely cause of syncope.