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Background: The diagnosis of acute ischaemic coronary syndromes in presence of an intra-ventricular conduction disturbance represents a clinical challenge. In the cardiac segmentation model the posterior wall is replaced by the basal inferior segment. However, in the clinical scenario of acute coronary syndrome the concept of posterior myocardial infarction (PMI) endures. The association of a PMI and right bundle branch block (RBBB) is a rare condition characterised by broad R waves and ventricular repolarization disorders in right precordial leads in both entities, which could lead to misinterpretation and delay in reperfusion therapy., Case Summary: We describe a case report of a 74-year-old man with acute chest pain and an electrocardiogram with broad R waves, a 4 mm ST-segment downsloping (excessively discordant) in right precordial leads, RBBB, and ST-segment elevation in posterior leads. There was resolution of ST-segment downsloping in right precordial leads after percutaneous coronary intervention and stenting of the circumflex artery, with disturbance of the repolarization process only attributable to RBBB., Discussion: Patients with acute chest pain with RBBB and a ST segment with an excessive downsloping (out of proportion of what is expected in isolated RBBB) suggest PMI with occlusion of the circumflex coronary artery.

Auscultation of the heart is a clinical art that allows the doctor to make accurate diagnoses with the skills after formal training. The technology efficiently complements the clinical diagnosis, so that the latter is insufficient without a clinical approach; on the other hand, when the clinical practice is replaced by technology, diagnosis and treatment is equally ineffective. The cult of technology has led to the gradual/ass of the ability of cardiac auscultation, and the doctor has lost a powerful tool with diagnostic potential.

One of the most common indications in echocardiography is the evaluation of left ventricular function. The traditional measurement of ejection fraction is based upon tracing the left ventricular borders and calculating left ventricular volumes using geometric assumptions. Now, with the introduction of three-dimensional echocardiography, the evaluation of left ventricular function is easier to carry out and with superior accuracy and reproducibility. However, regional myocardial function is more difficult to evaluate because it relies on visual assessment of endocardial motion and wall thickening. Currently, new techniques like tissue Doppler and speckle tracking imaging allow regional and global quantification of myocardial function through new parameters, like deformation/strain, rotation and twist. In this regard, speckletracking echocardiography (STE) has been introduced as a technique for angle-independent quantification of multidirectional myocardial strain and rotation. With the arrival of three-dimensional systems, the entire left ventricle can be evaluated with this technique, lacking the inherent weakness of two- dimensional and tissue Doppler methods. Three dimensional speckle tracking (3DST) has potential to be an ideal tool to assess not only global myocardial function but regional function through deformation, rotation, twist and untwisting parameters.

A complete ECG thoracic circle allows exploring some heart structures not explored by the conventional electrocardiogram. It provides a direct indication on the location of the damaged myocardium. In fact, posterolateral infarctions can be limited to the inferior third of the left ventricle or can cover the entire free left ventricular wall from the base up to the heart apex and can be univentricular or biventricular. On the other side, the unipolar thoracic leads and the high abdominal leads MD, ME, MI show the evolution of the signs of injury, characteristic of the acute stage of infarction, toward necrosis. We present the example of a 61-year-old man, whose ECG shows signs of subepicardial or transmural injury and of necrosis in the low precordial leads V5 and V6, as well as in the high left posterior leads V8 and V9. This fact suggests the presence of an acute extensive myocardial infarction extending from the base to the heart apex. Moreover, the moderate elevation of the RS-T segment from to V9R to V7R indicates the presence of subepicardial injury in the high posterior regions of the right ventricular wall. These electrocardiographic data were confirmed by the radioactive isotope study and, definitively, by the anatomical findings.

The purpose of this study is to calculate non invasivelly left ventricular systolic wall stress by echocardiography in patients with primary heart failure, and compare the results with those obtained in parients with overloaded heart failure, diastolic dysfunction by Inapropiatte hypertrophy, with normal ejection fraction and people with normal heart, there stablish the value of the results in clinical settings. We studied 33 patients with heart failure by dilated cardiomyopathy. There was no significant association between the systolic wall stress and the ejection fraction, fractional shortening, dp/dt or left ventricular mass in this group of study. There was a significant association between systolic h/r ratio and the systolic wall stress. This study shows that in primary heart failure the afterload increases and has inverse relationship with ejection fraction (r = 0.86); but, when heart failure obey to an excessive overload exists an exquisite inverse relationship between systolic wall stress and ejection fraction (r = 0.93). The excessive hypertrophy (Inappropriate) reduces the systolic wall stress but causes diastolic dysfunction. The increase of systolic wall stress in Aortic regurgitation with normal ventricular performance is responsible of adequate left ventricular hypertrophy, by other means, in mitral insufficiency the presence of low or normal systolic wall The purpose of this study is to calculate non invasivelly left ventricular systolic wall stress by echocardiography in patients with primary heart failure, and compare the results with those obtained in parients with overloaded heart failure, diastolic dysfunction by Inapropiatte hypertrophy, with normal ejection fraction and people with normal heart, there stablish the value of the results in clinical settings. We studied 33 patients with heart failure by dilated cardiomyopathy. There was no significant association between the systolic wall stress and the ejection fraction, fractional shortening, dp/dt or left ventricular mass in this group of study. There was a significant association between systolic h/r ratio and the systolic wall stress. This study shows that in primary heart failure the afterload increases and has inverse relationship with ejection fraction (r = 0.86); but, when heart failure obey to an excessive overload exists an exquisite inverse relationship between systolic wall stress and ejection fraction (r = 0.93). The excessive hypertrophy (Inappropriate) reduces the systolic wall stress but causes diastolic dysfunction. The increase of systolic wall stress in Aortic regurgitation with normal ventricular performance is responsible of adequate left ventricular hypertrophy, by other means, in mitral insufficiency the presence of low or normal systolic wall stress does not induce left ventricular hypertrophy, then diameter increases and the hypertrophy is inadequate, despite this, left ventricular function is normal.

Objective: To determine the systolic parietal stress of the left ventricle by image of magnetic resonance in healthy subjects., Material and Methods: 21 healthy subjects studied: 11 male and 10 female: the ages among 26 and 31 years (29.33). A magnetic resonance of heart was made using the short axis at the level of the papillary muscles, from where the epicardic and endocardic areas of the left ventricular cavity were obtained in diastolic as in systolic by means of the layout with an electronic pencil, later the radius of each drawn up area was calculated, with the value of the radius, the diastolic and systolic thickness was calculated; to obtain the relation between thickness/radio. Once the relation was obtained between thickness/radio in diastole as systole the degree of change between both values and the percentage of this change was calculated. Finally, the systolic parietal stress developed by the left ventricle was calculate with the following formula: S = PVI x A4/A3-A4 x 1.35.PVI: systolic pressure of the left ventricle (the average of 5 synchronized systolic arterial pressures, obtained by an esphingomanometer). A4: endocardic area in systole; A3: epicardial area in systole. The value obtained in this equation was multiplied per 1.35 to turn mmHg gm/cm2., Results: The average of the arterial systolic pressure was of 103.24 +/- 10.27 mmHg; A3 (average 27.58 +/- 2.29); A4 (average 6.84 +/- 0.71); being the systolic stress of the left ventricle of 46.12 +/- 4.9 gm/cm2, not existing significant differences between sexes., Conclusions: With this new method it is possible to determine with greater exactitude in a noninvasive way, through the best definition of its epicardic and endocardic edges, the areas and the radio of the left ventricular cavity in systole as in diastole, to determine the thickness of the wall and its relation with the radius, for one better valuation of the ventricular function, specially in those subjects with overloads of volume or pressure that depress the ventricular function.

This paper reviews the concepts of systolic function, diastolic function, heart failure, diastolic dysfunction, and diastolic heart failure. We refer to the historic evolution of the concept of heart failure and the origin of the term diastolic heart failure. Based on the current concepts of the physiology of the heart and its pathophysiology, we discuss the inappropriateness of the term and to the confusion it has generated in clinical practice, treatment, and prognosis, as well as in numerous research papers (of which some examples are given) when terming as "heart failure" the diastolic dysfunction and using both terms indistinctively. We conclude that an increasing need has arisen, ever more imperative, to identify clearly the concepts of heart failure and diastolic dysfunction, emphasizing on their differences to recognize them as distinct clinical entities with their own personality and, hence, having different prognosis and treatment. This would be of great help to achieve more accuracy in the clinical guidelines, standards, and consensus, especially regarding treatment. Besides it would be useful to avoid, inconsistencies in the design of research, which appear in some of the publications just by the lack of a clear meaning of the terms. Finally, at present we have the necessary elements to conclude that the terms "diastolic heart failure" and "cardiac failure with preserved systolic function" are inexact, poorly gauged, and far away from the actual problem they try to define. Therefore, they should be substituted by the concept of Diastolic Dysfunction, which defines clearly the pathophysiology of the functional alteration, without having to state that "the heart is failing".

The echocardiogram is an easily accessible procedure to study patients with heart disease. It is very useful specifically to establish a diagnosis of heart failure and to distinguish this condition from other diseases with similar clinical manifestations, which require different treatment and with distinct prognosis. Once the diagnosis has been established with certainty, other parameters must be obtained, such as ejection fraction, ventricular mass, mass/volume ratio, thickness/radius ratio (h/r), dP/dT of the left ventricle, and a recording of transmitral blood flow can be obtained by means of pulsed and continuous Doppler blood flow. All these measurements not only quantify the degree of heart failure but also have a powerful prognostic implications.

Better knowledge of mechanisms which perpetuate heart failure and promote progression and death in patients with these sicknesses, has led to find a better medical treatment to improve the functional status, decrease mortality and improve life span, avoiding the progression of ventricular dysfunction. Mortality reduction due to the disease progression has led to evident arrhythmic mortality show by sudden death. Aspects involved in the genesis and pathophysiology of sudden death in patients with chronic-heart failure; are reviewed in this paper. Special reference to mechano-electrical feedback is considered.