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A 70-year-old male presented to emergency room 16 h after the onset of acute chest pain. Initial ECG showed sinus rhythm with a wide QRS and right bundle branch block (RBBB) with concordant and symmetric T waves in V1-V2. A plausible explanation for the atypical positive T waves in leads V1-V2 in conjunction with RBBB could be non-reperfused lateral MI (LMI) as a "mirror-image" of inverted T waves in the posterior leads V7-V9. Coronary angiography showed total thrombotic occlusion TIMI thrombus grade 5 of the circumflex artery. One ECG expression of circumflex artery occlusion is isolated LMI., (Copyright © 2018 Elsevier Inc. All rights reserved.)

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.

The findings of the 1996 Cardiac Catheterization Laboratory Survey of the Sociedad Mexicana de Cardiología are presented. There are 52 cardiac catheterization laboratory departments distributed in 16 cities of which Mexico City has 20, Guadalajara 6 and Monterrey 5. Ninety-six percent are in hospitals where heart surgery can be performed and 8 (17%) have a training program in cardiac catheterization. Only two (3.8%) are exclusively dedicated to pediatric cardiac catheterization. In 1995, 19,214 diagnostic procedures and 2,429 PTCAs were done. A total of 270 physicians were reported to have privileges to perform cardiac catheterization. The geographical distribution of the cath labs, procedure volumes and number of physicians performing catheterization are discussed.

We studied 25 patients with hypertension documented through ambulatory blood pressure monitoring (ABPM) to know the antihypertensive effect of Lisinopril and its action throughout the day. ABPM was done in all patients after two weeks of washout (phase 1). Then patients took 20 mg daily of Lisinopril during four weeks and after that ABPM was repeated (phase 2). Finally, those patients who persisted with high blood pressure received 40 mg daily of Lisinopril during four more weeks and again ABPM was repeated (phase 3). We found statistic difference in the systolic and diastolic blood pressure among the three phases. During the first phase there were 17 patients (68%) with high blood pressure and this number decreased to 8 (32%) in the second one and to 7 (28%) in the third phase. The results show that Lisinopril has satisfactory antihypertensive effect in about 40% of patients. Nevertheless 20% of the case remained with high blood pressure despite treatment with 40 mg of Lisinopril. On the other hand, both, systolic and diastolic blood pressure decreased satisfactory during the night with the dosage received in the morning. We concluded that Lisinopril has moderate effect when it is given as monotherapy and, it has satisfactory effect all over the day.

We studied 300 patients (p) with dobutamine stress echocardiography (DSE) and atropine. The indication were chest pain, abnormal electrocardiogram (ECG), abnormal stress electrocardiogram with or without chest pain or any combination of these. The DSE was evaluated with digitized imaging in long and short parasternal views and apical four and two chambers views before and during dobutamine test with simultaneous side by side display. In 21 p (56.7%) we found positive concordance in diagnosis of coronary artery disease (CAD) between coronary arteriography (CA) and DSE. In 13 of 37 p the concordance was negative by the two methods (35.1%); then the DSE was capable correctly predict in 34 p (91%). The abnormal CA and normal DSE were found in one p (4.5%) with 90% obstruction of a small diagonal vessel. In two women DSE was abnormal with inferior hypokinesis (13.3%) and the CA was normal. In 43 p (14.3%) ECG and DSE were positive for myocardial ischemia (MI); negative concordance of both procedures was found in 203 p (67.6%). ECG was abnormal and DSE normal in 46 p (15.3%) 61 p (20.3%) with DSE abnormal in 8 p (2.6%) 61 p (20.3%) had arrhythmias; in 55 (18.3%) premature ventricular contractions, one p with ventricular tachycardia (0.33%); 7.3% of them required endovenous lidocaine. Chest pain was present in 22 p (7.3%) and the treatment waqs sublingual isosorbide; hypotension appeared in 27 p (9%) and were treated with saline infusion. Hypertensive response was found in two p (0.66%) and were treated with nifedipine and smolol. We concluded that DSE with atropine has high sensibility (95.5%) and specificity (86.6%) in the diagnosis of ischemic heart disease. The adverse effects are nondangerous and easily resolved with medical treatment.

We studied 60 people who were separated into three groups. Group A: 11 patients with pure, severe mitral regurgitation (MR); Group B: 18 patients with pure, severe aortic regurgitation (AR) [this group was divided into two: I) with normal ejection fraction (EF) and II) with low EF]. The third group was a control one with 31 healthy people. Through 2-D Echocardiography (2-D Echo) we got: diameters of the cavities, thickness of the wall, ventricular function, h/r ratio, and systolic wall stress (S). Patients with MR showed left atrial and ventricular enlargement with low h/r ratio, normal ventricular function and raised S. The group I of AR had left ventricular enlargement and hypertrophy, with normal h/r ratio and EF, and with raised S, while the group II of AR showed left ventricular enlargement, low h/r ratio and EF with very high S. In MR volumetric overload causes different anatomic and functional changes on the left ventricle than in the AR. In MR there is a systolic leak toward left atrium. This causes the low S in the beginning of the illness and is not the mechanism that trigger left ventricular hypertrophy (LVH). The absence of LVH causes excessive enlargement of the myofibril and with time there is structural damage and contractile failure which raises the systolic volume and S. Later on, hypertrophy develops. On the other hand, since the beginning AR has high S which causes adequate hypertrophy (normal h/r ratio) and later it produces huge ventricular enlargement decreases the h/r ratio (inadequate hypertrophy) with contractile failure. We conclude: the time of surgery in MR is when the patient raises S and in the AR when inadequate hypertrophy appears (low h/r) but when EF is still normal.

We studied 15 patients with essential hypertension (EH) in whom the diagnosis was corroborated with ambulatory blood pressure monitoring (ABPM). The blood pressure levels (BP) were compared with values obtained from healthy people (HP). We studied 31 HP with 2-D echocardiogram and the parameters of ventricular performance were compared with the values obtained from EH people. ABPM shown that the EH people has higher BP values than HP around 24 hs (EH loss the circadian rhythm of BP). On the other hand the EH had left ventricular hypertrophy (LVH) with normal systolic ventricular function (VF). The systolic wall stress was low because the LVH was inappropriate. The LVH as adaptative mechanism maintains normal the VF in spite of pressure overload without increasing MVO2. When the pressure overload is not eradicated in a variable amount of time the adaptative mechanisms slowly change to a pathologic process caused by collagen deposition in the interstitium of the heart. In advanced stages the remodeling process causes diastolic disfunction, myocardial ischemia, arrhythmias and death by heart failure or suddenly. This last stage is the real hypertensive heart disease.

For the purpose of evaluating the effectiveness of transdermal clonidine treatment (Catapres-TTS No. 2) on ameliorating withdrawal symptoms associated with smoking cessation, we carried out a prospective study on 375 patients who smoke, motivated to abandon smoking. Each patient acted as his own control at one moment receiving placebo and, at another, clonidine. Each patient was instructed to maintain his normal daily cigarette consumption during the first three days of study, and to stop smoking from the fourth to the seventh day. All of the withdrawal symptoms measured (craving, irritability, anxiety and restlessness) significantly increased (p = 0.001) in the placebo group during the days of abstinence. There was a 5 fold increase in craving and in irritability, in the placebo group, as compared with the transdermal clonidine group during the three days of smoking cessation. Anxiety and restlessness also augmented at 3 times greater extent. Regarding the side effects, these were slight and of a transitory nature. Transdermal clonidine treatment helps the heavy smoker to give up tobacco by means of a considerable drop of the short-term withdrawal symptoms, specially craving and irritability, associated with smoking cessation.

It is communicated an isolated mytral insufficiency case, secondary to thorax's penetrative wound by steel arm. There are commented the clinic discoveries, phonomechanocardiographic, echocardiographic, haemodynamic and operation results of a unique orifice in the mytral's septal valve with important overflow. When perforation was sutured it was necessary reoperate it in order to suture's dehiscence and valve's substitution by a Bjork-Shilley's prothesis. The patient persists asymptomatic 35 months after intervention.

The cause of an abnormal electrocardiographic P wave (AEPW) in systemic arterial hypertension (SAH) has not been delucidated. In order to demonstrate if this sign is related to volume overload of the left atrial cavity -previously we found no correlation between pressure overload of the cavity and the presence of an AEPW- 34 patients with SAH were studied; population were divided in two groups: group A (GA, n = 13), formed by 13 cases with a P wave more than 0.10 s duration (D2 standard lead) and group B integrated by 21 cases with a P wave at 0.10 s or less duration. In each cases phonocardiographic and echocardiographic (Mode M) studies were performed and the following data were obtained: "A" index (AI), left atrial dimension (LAD) and, septal (SD) and left posterior wall dimension (LPWD); besides: Sokolow electrocardiographic index (SI) and systolic (SBP) and diastolic (DBP) blood pressure. Results are shown in the following table: (Table: see text). There were not statistical differences between groups (data of SBP and DBP not shown). Correlation between LAD and AI and duration of P wave were not statistical different (data not shown). An AEPW in SAH does not seem to be cause by a volume left atrial overload. Possible it is related to an interatrial conduction defect.

We report a case of isolated aortic regurgitation complicated by active infective endocarditis with streptococcus viridans as causative organism. The affected structure was a previous normal mitral valve.