[Clinical interpretation for the pressure-flow relationships in extrinsic allergic alveolitis and in interstitial lung disease pulmonary hypertension patients. Should we care for the lung, the pulmonary artery pressure or both?]. / Interpretación clínica de la relación presión-flujo en enfermos con alveolitis alérgica extrínseca con neumopatía intersticial crónica e hipertensión pulmonar. Debemos tratar la hipertensión, la patología pulmonar o ambas?

OBJECTIVES: We sought to analyze exercise-derived mean pulmonary artery pressure (mPAP)-cardiac index (CI) relationship to expand the concepts regarding its nature and to better identify pulmonary hemodynamic responders to acute oxygen breathing (AO2B-99.5%) and to hydralazine (H) in extrinsic allergic alveolitis (EAA) and chronic interstitial lung disease (CILD) pulmonary hypertension (PH) patients. MATERIAL AND METHODS: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained while breathing room air (BRA) and under AO2B-99.5% in 38 stable (EAA (n = 14) and CILD (n = 24)) patients with resting and exercising PH. Hemodynamic characteristics were analyzed for the entire cohort and separate for EAA and CILD patients. AO2B-99.5% was tested in cohorts, H only in CILD and the effect of long-term corticosteroid treatment in EAA patients. Lung biopsies (LB) were obtained to evaluate the inflammatory-fibrosis stage and the degree of vascular lesion in the entire cohort. RESULTS: LB studies reveal a predominant stage of inflammation associated with grade-I vascular lesion for EAA patients. A predominant stage for fibrosis (although moderate) over inflammation associated with grade-II vascular lesions were documented for CILD patients. mPAP/CI abnormal location were associated with hypoxemia/decreased mixed venous-PO2 and lung mechanics abnormalities for both cohorts. An abnormal slope (Sp: 4.13; 95% CI: 3.42-4.84 mmHg/L/min/m2) and a normal Pext value (7 +/- 1.9 mmHg) were found for EAA patients. On the contrary, a normal slope (Sp: 1.22; 95% CI: 0.47-1.99 mmHg/L/min/m2) and an abnormal Pext value (19.7 +/- 3.5 mmHg) were found for CILD patients. Hemodynamic conditions that did not change for the Sp (4.0; 95% CI: 3.18-4.82 mmHg/L/min/m2); however, were associated with a statistical significant decrease in parallel for mPAP/CI during AO2B-99.5% when compared to BRA (p < 0.01), although not to normal slope values (0.96; 95% CI: 0.41-1.37) or mPAP/CI location. For CILD patients, during AO2B-99.5% no change for the slope, for Pext and mPAP/CI location in relation to BRA were observed. Under the effect of H, no change for the previous mentioned hemodynamic findings were found in relation to the control condition for CILD patients. After long-term corticosteroid treatment, normalization for mPAP/CI location and for the slope value (1.6; 95% CI: 0.91-2.29 mmHg/L/min/m2) were associated with lung mechanics and blood-gas exchange normalization were documented in EAA patients. CONCLUSIONS: When mPAP/CI exercise derived is analyzed, valuable information for linear-pulmonary vascular resistance-(LPVR) could be obtained for EAA and CILD-PH patients. mPAP/CI-r abnormalities not always reflect "pure arteriolar" increased LPVR for EAA and CILD patients. H is not useful as an adjunct vasodilator therapy for CILD-PH patients. AO2B-99.5% decrease right ventricular afterload for EAA patients, although not to normal. Complete reversibility for PH could result after long-term corticosteroid treatment. We conclude that treatment should focus mainly on the lung and not in the pulmonary artery pressure in interstitial lung disease PH patients.

Polymorphisms C677T and A1298C of MTHFR Gene: Homocysteine Levels and Prothrombotic Biomarkers in Coronary and Pulmonary Thromboembolic Disease.

The activity of the enzyme methylenetetrahydrofolate reductase (MTHFR) determines homocysteine (Hcy) levels, and polymorphisms in its gene affect the activity of the enzyme. Changes in the enzyme's activity may lead to a higher susceptibility to develop arterial and venous thromboembolic disease. The aim was to analyze the relationship between the C677T and A1298C polymorphisms of MTHFR, Hcy levels, and prothrombotic biomarkers in pulmonary embolism (PE) and acute myocardial ischemia (AMI). Clinical files of patients with thromboembolic diseases having complete data and whose doctor had requested an assay to determine the polymorphisms of the MTHFR gene, Hcy levels, and prothrombotic biomarkers were studied to search for the correlation between mutations of the MTHFR gene and Hcy levels in the different diseases. We included 334 files: 158 were from women and 176 from men (51 [19 SD] years). Sixty-three percent have had thrombosis, 8% AMI, and 31% PE. Patients with thrombosis had elevated frequency of the C677T polymorphism. The CC genotype was higher than the TT genotype ( P = .003) and CT versus the TT ( P = .009). In patients with PE, the CC genotype was higher than the TT genotype ( P = .038). Pulmonary embolism with massive and submassive events had predominant genotypes 677 TT ( P = .003) and the AA 1298 ( P = .017). Elevated Hcy levels in the presence of the T allele in the C677T gene and of the A allele in the A1298C gene are associated with AMI and massive and submassive PE.

A proposed functional clinical classification predicts in-hospital and long-term survival in the setting of acute right ventricular infarction.

BACKGROUND: The objectives of the present investigation were to validate the prognostic role of a proposed Clinical Classification [CC], to evaluate the TIMI risk score [RS] and to establish whether the TIMI-RS should incorporate points for patients with acute right ventricular infarction [TIMI-RS-RVI]. METHODS AND RESULTS: A total of 523 RVI patients were classified on clinical and functional basis as: A, without right ventricular failure [RVF], B with RVF and C with cardiogenic shock. The CC was evaluated prospectively among 98 patients with RVI and retrospectively in 425 RVI patients. The TIMI-RS was evaluated prospectively among 622 patients with STEMI [anterior:277, inferior:247, RVI:98], and retrospectively in 425 RVI patients. The CC established differences among the 3-RVI Classes for in-hospital mortality [prospectively and retrospectively; p<0.01, p<0.001, respectively] that were maintained at 8 years [p < 0.001]. Patients with anterior and inferior STEMI, but not those with RVI revealed an association between outcome and TIMI-RS [p<0.001]. Testing for TIMI-RS-RVI did not result a good prognostic tool [ROC=0.9; excellent discrimination, but with a very poor "clinical calibration"]. CONCLUSIONS: The proposed CC allowed prediction of mortality at short- and long-term in the setting of acute RVI. The role of the TIMI-RS should be reevaluated prospectively as a prognostic tool in the scenario of RVI patients.

[Staging imagenology in coronary syndromes]. / Optimización de los recursos de la imagenología en la cardiopatía isquémica.

For the physician, it should stand out very clearly that the clinical and rationale analysis of the symptoms observed in every patient suffering from stable chronic ischemic cardiopathy (SCIC) or acute coronary ischemic syndrome (ACIS), are the starting point to apply the available resources in imagenology, in order to apply in an optimized and sequential manner to stratify, without forgetting its inherent limitations, or identify its risk. This approach may be based on the ethics, with special emphasis on the patient economy, which may promote the use of indissoluble medical principles regarding never damaging, but improving, the survival. SCIC and ACIS prevalence is still very high in its actually recognized clinical-pathological avenues.

[Homeometric autoregulation in the heart. The Anrep effect. Its possible role in increased right ventricular afterload pathophysiology]. / La autorregulación homeométrica. El efecto Anrep. Su posible importancia en la patofisiología en los aumentos de la postcarga del ventrículo derecho.

One type of intrinsic response exhibited by the isolated and non-isolated heart is the well-known Frank-Starling mechanism, which endows the ventricles with performance characteristics such that the heart ejects whatever volume is put into it [heterometric autoregulation]. A second type of autoregulation in the isolated and no-isolated heart, one which apparently does not utilize the Frank-Starling mechanism, will be the main subject of this review. It requires at least a few beats to develop fully after an increase in activity. The ventricle then exhibits performance characteristics such that its end-diastolic pressure and fiber length tend to be maintained because of an increase in myocardial contractility. It will, therefore be referred to as homeometric autoregulation or Anrep effect. Assessment of ventricular load-independent parameters, including myocardial contractility, is important to better understand the pathophysiology of acute and right ventricular increased afterload. The role of the Anrep effect, in right ventricular dysfunction in patients with primary or secondary forms of pulmonary artery hypertension with chronic cor pulmonale, is analyzed and presented as an hypothesis to be considered in the pathophysiology in acute and in chronic states of right ventricular afterload.

[Clinical stratification of cardiogenic shock]. / Estratificación clínica del enfermo con estado de choque cardiogénico, el valor agregado del poder cardíaco y del índice de las resistencias periféricas.

Cardiogenic shock (CHC) associated to acute myocardial infarct has high mortality and their manifestations are heterogenous. In our institution historical mortality, was 98%, but with different methods of reperfusion, its reduced to 53%. In other hand, with opportune clinical stratification is useful to improve the treatment strategy. This stratification on basis in clinical signs: age, infarction location, cardiac frequency and systemic arterial pressure, and hemodynamical valuation with the use of right catheterism with quantification miocardial work parameters like "Cardiac power" that is the product of flow and arterial pressure and that is of utility to know the "Miocardial reserve". In our experience after reperfusion procedure patients with CHC and cardiac power less than 1.0 had highly mortality.

[From the single vulnerable plaque, to the multiple complex coronary plaques. From their basis, to the modern therapeutic approach. A clinical reality in the spectrum of the acute coronary syndromes]. / De la placa vulnerable solitaria, a la coronariopatía de multiples vasos. De sus fundamentos, a las implicaciones terapéuticas modernas. Una realidad clínica en el espectro de los SICA.

Contemporary clinical and laboratory data have challenged our classical concepts of the pathogenesis of the acute coronary syndromes [ACS]. Indeed, several independent lines of clinical evidence have supported that the critical stenoses cause only a fraction of the ACS. Acute myocardial infarction is believed to be caused by rupture of a vulnerable coronary-artery plaque that appears as a single lesion on angiography. However, plaque instability might be caused by pathophysiologic processes, such as inflammation, that exert adverse effects throughout the coronary vasculature and therefore result in multiple unstable lesions. Recent studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some ACS patients. It has also been reported that a ruptured plaque at the culprit lesion is associated with elevated C- reactive protein and other inflammatory markers, which indeed indicate a poor prognosis in patients with ACS. Also, multiple plaque rupture is associated with systemic inflammation, and patients with multiple plaque rupture can be expected to show a poor prognosis. Therefore some ACS patients [20-40%] may harbor multiple complex coronary plaques that are associated with adverse clinical outcomes. It should be accepted that this ACS population represent a part of the spectrum of the ACS, and in particular in this group of patients treatment should focus not only on the stabilization of the culprit site but also warrants a broader approach to systemic stabilization of the arteries. However, recurrent cardiovascular events in this population still remain unacceptably high, indicating that plaque rupture or vulnerability of multiple plaques is a current challenge in the management of ACS patients.

[From the single vulnerable plaque, to the multiple complex coronary plaques. From their basis, to the modern therapeutic approach. A clinical reality in the spectrum of the acute coronary syndromes]. / De la placa vulnerable solitaria, a la coronariopatía de múltiples vasos. De sus fundamentos, a las implicaciones terapéuticas modernas. Una realidad clínica en el espectro de los SICA.

Contemporary clinical and laboratory data have challenged our classical concepts of the pathogenesis of the acute coronary syndromes [ACS]. Indeed, several independent lines of clinical evidence have supported that the critical stenoses cause only a fraction of the ACS. Acute myocardial infarction is believed to be caused by rupture of a vulnerable coronary-artery plaque that appears as a single lesion on angiography. However, plaque instability might be caused by pathophysiologic processes, such as inflammation, that exert adverse effects throughout the coronary vasculature and therefore result in multiple unstable lesions. Recent studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some ACS patients. It has also been reported that a ruptured plaque at the culprit lesion is associated with elevated C- reactive protein and other inflammatory markers, which indeed indicate a poor prognosis in patients with ACS. Also, multiple plaque rupture is associated with systemic inflammation, and patients with multiple plaque rupture can be expected to show a poor prognosis. Therefore some ACS patients [20-40%] may harbor multiple complex coronary plaques that are associated with adverse clinical outcomes. It should be accepted that this ACS population represent a part of the spectrum of the ACS, and in particular in this group of patients treatment should focus not only on the stabilization of the culprit site but also warrants a broader approach to systemic stabilization of the arteries. However, recurrent cardiovascular events in this population still remain unacceptably high, indicating that plaque rupture or vulnerability of multiple plaques is a current challenge in the management of ACS patients.

[Reperfusion and postconditioning in acute ST segment elevation myocardial infarction. A new paradigm for the treatment of acute myocardial infarction. From bench to bedside?]. / De la reperfusión al post-acondicionamiento del miocardio con isquemia prolongada. Nuevo paradigma terapéutico de los síndromes coronarios agudos con elevación del segmento ST? De lo básico a lo clínico.

After prolonged periods of ischemia and energy depletion, the ischemic myocardial cell can be jeopardized by specific causes within the reperfusion period. These causes can be viewed as unwanted aspects of the recovery process itself limiting its efficiency. Three potential initial causes of immediate reperfusion injury, aside from oxygen radicals, have been experimentally investigated in detail, and are briefly discussed: 1. re-energization; 2. rapid normalization of tissue pH; and 3. rapid normalization of tissue osmolality. These potential causes are not entirely independent. Understanding of the basic causes has opened novel perspectives for specific interference with these serious pathomechanisms. The experimental results obtained in the last years encourage the development of therapeutic approaches to reduce infarct size by specific measures applied during the early phase of reperfusion. In the clinical setting, reperfusion therapy for acute myocardial infarction (AMI) has shown to reduce mortality, yet it may also have deleterious effects, including myocardial necrosis and no-reflow. Almost two decades ago, great hope arose from the description of ischemic preconditioning. Unfortunately, ischemic preconditioning is not feasible in the clinical practice because the coronary artery is already occluded at the time of hospital admission of the AMI patient. Recently, in the dog model, a phenomenon called "postconditioning" has been described. It has been reported previouly that reperfusion injury can be significantly reduced by modifying the conditions and the composition of the initial reperfusate. Whereas preconditioning is triggered by brief episodes of ischemia-reperfusion performed just before a prolonged coronary artery occlusion, postconditioning is induced by a comparable sequence of reversible ischemia-reperfusion, but it is applied "just after the prolonged" ischemic insult. Protection afforded by postconditioning is as potent as that provided by preconditioning. Unlike preconditioning, the experimental design of postconditioning allows direct application in the clinical practice, especially during PTCA. It has been reported very recently, that postconditioning patients with ST segment elevation AMI, during coronary angioplasty protects the human heart in this clinical scenario. Obtaining such a beneficial effect by a simple manipulation of reperfusion is of major potential clinical interest. Now more than ever, mechanistic and pharmacological research in the field of reperfusion injury appears to be necessary and clinically relevant.

["Cardiac power output" an old tool, possibly a modern tool for assessing cardiac pumping capability, as well as for a short-term prognosis in cardiogenic shock due to acute myocardial infarction]. / "ll poder cardíaco" un instrumento del pasado, posiblemente una herramienta moderna en la valoración: clínica, terapéutica y pronóstica del choque cardiogénico por síndrome isquémico coronario agudo.

Hemodynamic monitoring has been used extensively during the last decades for risk stratification and guiding treatment of patients with cardiovascular destabilization, especially in the scenario of acute heart failure and cardiac shock. Every cardiac pump has its own maximum performance, which denotes its pumping capability. The heart is a muscular mechanical pump with an ability to generate both flow (cardiac output) and pressure. The product of flow output and systemic arterial pressure is the rate of useful work done, "or the cardiac power" (CP). Cardiac pumping capability can be defined as the cardiac power output achieved by the heart during maximal stimulation, and cardiac reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state (CPR). Resting CP for a hemodynamically stable average sized adult is approximately 1 W. However, during stress or exercise, CPR can be recruited to increase the heart's pumping ability up to 6 W. In acute heart failure, the patient becomes hemodynamically unstable, and most of the cardiac pumping potential is recruited in order to sustain life. Hence, cardiac power measurements in patients with acute heart failure or with cardiogenic shock at rest represent most of the recruitable reserve available during the acute event, and their measurement reflects the severity of the patient's condition. It has been found that a cutoff value for CP of 0.53 W accurately predict in-hospital mortality for cardiogenic shock patients. Others investigators observed cutoff for increased mortality of CP < 1 W, data that were obtained at doses of maximal pharmacologic support yielding the individual maximal CP. In our experience, the cutoff value for CP that accurately predicts in-hospital mortality for cardiogenic shock patients is 0.7 W, but its impact on short-term prognosis is clearer if the patient achieves a CP equal or higher than 1 W after an optimal myocardial revascularization with interventional cardiac procedures. According to the data collected from the literature, CP deserves a place in the evaluation of the patient with cardiogenic shock due to an acute myocardial infarction, but a more profound analysis of this parameter an further evaluation are required in order to better understand its prognostic meaning in this acute cardiac syndrome.

Risk factors, echocardiographic patterns, and outcomes in patients with acute ventricular septal rupture during myocardial infarction.

Ventricular septal rupture (VSR), which can complicate an acute myocardial infarction (MI), carries a high mortality rate. Because precordial and transesophageal echocardiography can identify the type of rupture and assess right ventricular (RV) function at the patient's bedside, we examined the prognostic significance of echocardiographic patterns in postinfarct VSR by postulating that complex rupture and RV involvement carry a worse prognosis. Seventeen patients (10 men; mean age 66 years) who had confirmed postinfarct VSR underwent precordial and transesophageal echocardiography followed by coronary angiography. Serial 12-lead and right precordial leads were also available. Type of septal rupture was classified as simple or complex based on autopsy-proved echocardiographic criteria. Three patients had inferior wall MI and 14 had anterior wall MI. ST-segment elevation persisted >72 hours in all 3 patients who had inferior wall MI and in 12 who had anterior wall MI. Segmental wall motion abnormalities helped in detecting the left ventricular entry site, and use of unconventional views superimposed with color flow Doppler provided the RV exit site. RV function was better appreciated with transesophageal echocardiography. Two patients who had inferior wall MI and 7 who had anterior wall MI had complex ruptures. All 3 patients who had inferior wall MI and 7 who had anterior wall MI had electrocardiographic and echocardiographic evidence of RV involvement. Mortality rate was higher in patients who had complex rupture (78% vs 38%, p <0.001) and in those who had RV extension (71% vs 29%, p <0.001). In conclusion, persistent ST elevation is a common finding in patients who have postinfarct VSR. Complex VSR and RV involvement are significant determinants of clinical outcome.

[Mortality in cardiogenic shock]. / Choque cardiogénico. Las variables de mortalidad.

OBJECTIVE: Cardiogenic shock (CS) is one of principal causes of mortality after an acute myocardial infarction (MI). The objective of this study was to determine the principal causes that contribute to an increase in mortality in CS. METHODS: We studied 155 consecutive patients with CS admitted to the Coronary Care Unit of the Instituto Nacional de Cardiologia Ignacio Chávez from 1990-2002. RESULTS: Patients older than 60 years with MI and diabetes mellitus presented a higher cardiovascular mortality (p<0.001). Percutaneous coronary intervention (PCI) procedures decreased the cardiovascular mortaly in CS as compared to those patients not submmitted to PCI (59% vs. 98%, p<0.001). CONCLUSIONS: Mortality due to CS is still very high (80%). Previous MI and diabetes favor short-term mortality and the use of PCI suggests a clinical favourable trend in the reduction of mortality due to CS. PCI appears to be the most appropriate reperfusion procedure for treating CS.

Prevalence of Congenital Heart Disease and Pulmonary Hypertension in Down's Syndrome: An Echocardiographic Study.

BACKGROUND: Down's syndrome (DS) is a genetic anomaly, which undergoes increased morbidity and mortality when associated with congenital heart disease (CHD). The aims of the study were to determine the prevalence of CHD and pulmonary hypertension (PH) in DS. METHODS: One hundred twenty-seven patients with DS living in Mexico City were evaluated by physical exam, electrocardiogram and echocardiogram. RESULTS: CHD was found in 40%. In 80% (n = 102) PH was present [systolic pulmonary artery pressure (SPAP) of 47 ± 19 mm Hg and mean pulmonary artery pressure (MPAP) of 32 ± 11 mm Hg]. Patients with CHD and PH were classified as having 1) no shunt (n = 18) with SPAP of 37 ± 9 mm Hg and MPAP of 25 ± 6 mm Hg and 2) with shunt (n = 26) with PASP of 57 ± 29 mm Hg and MPAP of 38 ± 19 mm Hg (p ≤ 0.001). In those without CHD or with CHD without shunt (n = 76), SPAP was 37 ± 19 mm Hg and the MPAP 25 ± 6 mm Hg. The prevalence of PH in DS was 5.9% at one year and 15% at 10 years. The odds ratio of PH in DS with CHD was 7.3 vs. 3 without CHD. CONCLUSION: DS has a high prevalence of CHD and PH. PH prevalence increases when it is associated with CHD. The pathophysiology of PH in DS without CHD should be studied in the near future. Echocardiography is an indispensible tool for evaluation of DS.

Acute right ventricular infarction: clinical spectrum, results of reperfusion therapy and short-term prognosis.

BACKGROUND: The role of thrombolytic therapy (TT) and percutaneous coronary interventions (PCIs) in subgroups of patients with right ventricular infarction (RVI) has not been evaluated. METHODS AND RESULTS: We risk-stratified 302 patients with RVI into three subsets upon admission. Class A (n=197) comprised patients without right ventricular (RV) failure, Class B (n=69) with RV failure and Class C (n=36) with cardiogenic shock. All eligible patients in Class A or B received either PCI or TT. Patients in Class C eligible for reperfusion were treated with PCI. All patients were evaluated for in-hospital major adverse cardiac events and short-term mortality. There was a statistically significant difference in in-hospital mortality among the classes. Classes B and C were the strongest indicators of in-hospital mortality. By multivariate analysis TT or PCI did not reduce mortality in Classes A and B, but a clinically favorable trend in mortality reduction was documented: both methods decreased RV dysfunction in Class B (from 97% to 61% with TT and to 28% with PCI; P < 0.001) and PCI reduced the risk of mortality in Class C (89.5% compared with 58%; P < 0.05). CONCLUSIONS: Classification into types A, B or C allows the prediction of mortality. The use of TT or PCI suggests a clinical favorable trend in the reduction of mortality in Class A, either is beneficial in Class B for decreasing morbidity and PCI appears to be the most appropriate procedure for Class C since it reduced mortality.

Clinical-Echocardiographic Correlation of Myocardial Infarction with Extension to Right Chambers.

In order to determine the transesophageal echocardiographic characteristics in patients with acute myocardial infarction of right ventricle and establish the relationship between these findings, the clinical condition, and their prognostic value, 38 patients consecutively admitted to the Instituto Nacional de Cardiología with a diagnosis of acute left ventricular myocardial infarction with extension to right ventricle and/or atrium were retrospectively studied. Of the left ventricular infarctions, 37 were posteroinferior and one anterior. Significant elevations of CPK and DHL were found in 35. In 30 patients (78%) electrocardiographic evidence of extension of infarction to the right ventricle was found, and in 3, evidence of right atrial infarction. Twenty-one patients presented clinical data compatible with right ventricular infarction. In 19, cardiac rhythm and atrioventricular conduction disturbances were documented. Coronary angiograms practiced on 34 patients demonstrated single-vessel (right coronary) disease in 12, affection of two vessels in 14, and lesions in three or more in 6. Coronary arteries presented no significant lesions in two cases. With TEE, alterations of right ventricular segmental mobility were demonstrated in all patients, and in 6, alterations of right atrial mobility as well. As respects the ventricular wall movement index, 68.5% had total scores (RV + LV) of <5. The other 31.5% had scores >/= 5. In 26%, the right ventricular wall movement index was >/=4. The RVDD/LVDD ratio was 1 or less in 30 patients (78%) and >1 in only 8 (22%). The conclusions from these findings are that: (1) TEE is an excellent diagnostic means of identifying right ventricular and/or atrial infarction; and (2) a relationship exists between the magnitude of right ventricular damage and a wall movement index of 5 or more or an RV/LV diastolic diameter ratio > 1:postinfarction hemodynamic deterioration is significantly greater and the incidence of intrahospitalary complications higher.

Multiplane Transesophageal Echocardiography with Dobutamine in Patients with Biventricular Inferior Myocardial Infarction.

The purpose of this study was to evaluate the alterations of ventricular wall movement in patients with acute posteroinferior myocardial infarction with extension to right cavities with multiplane transesophageal echocardiography (TEE), as well as the utility of dobutamine with this technique to analyze myocardial viability. Nine men with a mean age of 51 years fulfilled the inclusion criteria. Myocardial TEE was performed in all the men 72 hours after the acute event with long- and short-axis transgastric images of both ventricles under basal conditions and with dobutamine infusions of 5 and 10 µg/kg per minute. Results were compared with myocardial perfusion findings obtained with Tc-99m Sestamibi SPECT. Left ventricular myocardial viability was demonstrated in 28 of 45 altered segments with dobutamine stress myocardial TEE and Tc-99m Sestamibi SPECT. Right ventricular myocardial viability was identified in 27 of 30 altered segments with dobutamine stress myocardial TEE in transgastric short and long axes, and with Tc-99m Sestamibi SPECT in 23 of 25 segments only in short-axis images. Multiplane TEE provided excellent image resolution and better definition of endocardial and epicardial borders, which facilitated detailed evaluation of ventricular segmental wall movement. Infusion of low doses of dobutamine made it possible to identify viable tissue in both ventricles, and results were comparable to those of nuclear medicine.

Transesophageal Echocardiographic Study of Right Atrial Myocardial Infarction and Myocardial Viability.

In order to determine the effects of dobutamine on right atrial wall movement, two groups were studied using transesophageal echocardiography. Group A included six patients without ischemic heart disease. Group B included six patients with infarction of the inferior wall of both ventricles and abnormal wall movement of the right atrium. In group A, an increase in the amplitude of right atrial movement was observed with dobutamine at doses of 5 and 10 µg/kg per minute. In group B, infusion of dobutamine did not modify wall akinesis in three patients with right atrial infarction; in the remaining three, alterations of segmental atrial movement were evident, and their responses to dobutamine were related to the patency of right atrial coronary branches. The following conclusions were reached: (1) dobutamine has a positive inotropic effect on atrial myocardium; (2) right atrial ischemia appears in the echocardiogram as altered segmental or global wall movement; (3) dobutamine can be used in the evaluation of atrial myocardial viability.

Experimental Right Atrial Ischemia and Its Response to Stimulation with Dobutamine.

In order to analyze the repercussion of experimental isolated selected right atrial ischemia on the hemodynamics of both ventricles, we investigated the response of atrial myocardium with administration of dobutamine and evaluated the utility of transesophageal echocardiography (TEE) with Doppler in the examination of alterations produced by atrial ischemia. Ten dogs were studied with normal, diminished, and increased cardiac output with ligation of the visible atrial branches of the right coronary artery. Right atrial wall movement and peak A wave velocity of tricuspid flow registered by TEE decreased (P < 0.05). The amplitude of the right atrial A wave decreased in hemodynamic recordings (P < 0.05). No significant modifications occurred in right ventricular wall movement nor in pressures registered in right or left ventricles or cardiac output. Seventy-five minutes after atrial ischemia was induced dobutamine was administered. In dogs with incomplete ligations of atrial circulation, right atrial wall movement improved (P < 0.001), and the amplitude of the peak A wave velocity of tricuspid flow increased. In dogs with complete coronary ligation, administration of the medication produced no improvement of these variables. The findings indicate that it is possible to produce selective right atrial ischemia manifested by diminished wall movement, a diminished atrial component of tricuspid flow in TEE, and decreased amplitude of the A wave in atrial pressure recordings. The localized hemodynamic changes produced by right atrial ischemia are not related to variations in venous return when right ventricular function is normal. Apparently isolated right atrial damage from ischemia does not affect ventricular function if these remain healthy. The recuperation of atrial contractility can be demonstrated with dobutamine. Transesophageal echocardiography is a very useful technique for studying right atrial ischemia and infarction.

[National Registry of Acute Ischemic Coronary Syndromes (RENASICA). Mexican Cardiology Society. The RENASICA Cooperative Group]. / El Registro Nacional de los Síndromes Isquémicos Coronarios Agudos [RENASICA] Sociedad Mexicana de Cardiología. Por el Grupo Cooperativo RENASICA [+].

This study assessed current practices in relation to coronary risk factors, therapy and its results in patients with acute ischemic coronary syndromes (AICS) with or without ST-segment-elevation myocardial infarction [MI], from data collected in the National Registry of AICS [RENASICA] in México; Eigh teen hospitals [2nd. and 3rd level of medical attention] recruited patients for the registry, 4,253 patients were enrolled, 2,773 [65.2%] without AICSST segment elevation and 1480 [34.8%] patients with ST segment elevation MI. Chest pain was the main cause for seeking medical attention to an emergency service (90.5%) and 50% of the patients referred it in advance. AICS was mainly observed in men in their sixth decade of age. Age, ST segment depression [> 2 mm], CKMB [> 2 values above normal] and the extension of the coronary artery disease allow to predict mortality and the combination of mortality and myocardial infarction. Only 50.4% of the eligible patients with AICS and ST-segment-elevation myocardial infarction received thrombolytic therapy. Of the eligible cohort of AICS only 58% patients could an hemodynamic study be performed. In 55% of them, a percutaneous coronary intervention procedure was done (PTCA-Stent implantation). Aspirin [ASA] and heparin were prescribed in 70% of the patients at entry to the ward and the same percentage of AICS patients received ASA after discharge. Low molecular weight heparin and IIb/IIIa receptor platelet antagonists were used in a low proportion of patients. RENASICA provides information related to AICS patients that could help the mexican health authorities to apply better the health resources in the forthcoming future for the treatment of AICS.