[Influence of the pericardium in the pathophysiology of ventricular dysfunction in acute infarct of the right ventricle. Experimental study] . / La influencia del pericardio en la patofisiología de la disfunción ventricular en el infarto agudo del ventrículo derecho. Estudio experimental.

UNLABELLED: To obtain more information about the role of the pericardium in the setting of acute right ventricular infarction (ARVI) we studied the behaviour of the ventricular function curves (VFC) and the relationship of the ventricular end-diastolic pressures (R-VEDP-RV:LV) in two groups of dogs. Group A. (n = 12) Control (C), ARVI, Pericardiectomy (P). A parabolic behaviour of the C VFC was noted (r2 = 071) and it's flexion point (FP) was found in 13. +/- 2 mmHg. After the ARVI the right (R) VFC was shifted downwards and to the right and the FP was documented in 18 +/- 2 mmHg (p < 0.05) in relation to C VFC. After P the RVFC was displaced upwards and to the left in relation to ARVIC RVFC (p < 0.05). The C R-VEDP-RV:LV = 0.75 and only a trend to equalization after the ARVI and after P were noted (0.91, 0.84, respectively) (p = ns). Group B (n = 12). Control (C), P, ARVI. The RVFC after P was shifted up and to the left in relation to the C RVFC (p < 0.05) and the FP = 10 +/- 2 mmHg. After P in the setting of ARVI the RVFC was shifted downward and to the right in relation to P RVFC (p < 0.05). After P the R-VEDP-RV:LV = 0.45 and statistical significant equalized in the condition of ARVI without pericardium (0.95, p < 0.05). CONCLUSION: Ours results support a partial restrictive role of the pericardium in the origin of the low cardiac output (LCO) in ARVI. Because, equalization of the R-VEDP-RV:LV is not only due to the restraining pericardial effect but is also due to right ventricular myocardial ischemia. The FP (18. +/- 2 mmHg) found seems to be the top value of RVEDP for volume infusion in experimental ARVI. Hemodynamic finding that could be useful in the preload volume management for humans with ARVI and LCO or systemic hypotension.

[Ventricular function curves with and without pericardium: analysis of pericardial pressures]. / Las curvas de función ventricular con y sin pericardio: análisis de las presiones pericárdicas.

Simultaneous right and left ventricular function curves (VFC, R, L) were obtained in a canine model, (open chest preparation), with and without pericardium. Preload and afterload conditions for the right and left ventricles were controlled. VFC were constructed from zero to 25 mmHg of ventricular end-diastolic pressures and by increasing the cardiac output from 50 to 250 mL/kg-1min-1. Both, right and left VFC showed an initial steep rise at low filling pressures and then flattened off to a plateau at high filling pressures. The best mathematical model that fitted with the VFC, with and without the pericardium was the parabola (r2 = 0.71, 0.72 respectively). After pericardiectomy R and L VFC were displaced to the left of the VFC with pericardium and a decrease in filling pressures were noted at the same points of cardiac output, findings that suggest a restraining effect of the pericardium. By subtracting the filling pressures obtained with pericardium from those without pericardium at the same levels of cardiac output, pericardial pressures were derived. In all the range of the VFC the pericardial pressures were positive, and this pressure increase as cardiac output increase. Thus the transmural pressure was never cero, for both right and left ventricles. The observed relation for the R and L filling pressures, derived from a polynomial equation of second order suggest a small although not unimportant effect of the pericardium at normal filling pressures, and a very substantial influence at high levels of cardiac output. The demarcation between small and major effects appears in the upper range of normal filling pressures in this dynamic approach of the pericardial pressures.

Myocardial perfusion scintigraphy (SPECT) in the evaluation of patients in the emergency room with precordial pain and normal or doubtful ischemic ECG. Study 60 cases.

OBJECTIVES: To evaluate the diagnostic utility of myocardial perfusion by SPECT and Gated-SPECT in the diagnosis of acute coronary syndrome in patients with precordial pain associated with normal or doubtful ischemic ECG within the first 6 hrs of the last episode of pain. METHODS: Sixty such patients who sought attention in the Emergency room were included. Myocardial perfusion SPECT and Gated-SPECT (GSPECT) was performed in all patients using two distinct protocols. All patients underwent resting and pharmacological stress test. In 30 cases coronary angiogram were performed. RESULTS: Resting myocardial perfusion was abnormal or positive in 25 patients (42%) and normal or negative in 35 patients (58%). In the latter group perfusion became abnormal in 15 patients (43%) under stress with dipyridamole, while it remained normal in 19 (54%). The last subgroup presented no coronary events during the 12 months following their hospital discharge. In the group of 25 patients with resting perfusion abnormalities acute myocardial infarction was diagnosed in 7 patients, ischemia in 12 and reverse-reversibility in 6. Myocardial perfusion scintigraphy showed in the resting phase a low sensitivity of 61% (95% CI 39-74%), and negative predictive value of 71% (95% CI, 58-82%). During the stress phase, the utility of the test increased significantly, with a sensitivity of 97% (95% CI, 83-99%), specificity of 79% (95% CI, 57-92%), positive predictive value of 87% (95% CI, 72-95%) and, most outstanding, a negative predictive value of 95% CI, 73-99%). CONCLUSIONS: Myocardial perfusion studies have a sensitivity of 97% for identifying patients with acute coronary syndrome, with precordial pain and normal or doubtful ischemic ECG. For the intermediate or low risk patients with acute coronary syndrome the non-invasive diagnostic techniques of SPECT and GSPECT systems of evaluating myocardial perfusion achieve a high degree diagnostic accuracy, safety and reduces unnecessary admissions and costs.

[Late thrombolysis and electrical stability in acute myocardial infarction. Role of the collateral flow]. / Trombolisis tardía y estabilidad eléctrica en el infarto agudo del miocardio: importancia del flujo colateral.

We evaluated 249 patients (pts) with first acute myocardial infarction: 1. Pts without thrombolysis, n = 119, 2. Pts treated with thrombolysis within 6 hours following MI, n = 80 and 3. Pts treated with thrombolysis between 6-12 hours after MI. Arrhythmic events were evaluated during follow up. All underwent heart rate variability studies and coronary angiogram where anterograde flow (TIMI) and collateral flow (Rentrop scale 0-2 = poor collateral flow and 3 = good collateral flow) were determined. Pts in group 2 and 3 showed a better anterograde and collateral flow than group 1 (p < 0.001). A lower spectral power in the high frequency band and a higher ratio low/high frequency band were observed in group 1 (p < 0.05). Conjunctive consolidation analysis showed more malignant arrhythmias in TIMI 0-2 with poor collateral flow than TIMI 0-2 with good collateral flow (17/138-12.3% vs 0/14-0%). Kaplan Meier analysis was able to demonstrate more cardiac sudden death events in TIMI 0-2 with poor collateral flow than TIMI 0-2 with good collateral flow or TIMI 3 (x2 = 7.22, p = 0.028), independently of thrombolytic treatment.

[Results of treatment of acute myocardial infarction with thrombolytic therapy. Experiences in 437 patients in the coronary care unit of the National Institute of Cardiology "Ignacio Chavez"]. / Resultados del enfermo con infarto agudo del miocardio con terapia trombolítica. Experiencia en 473 enfermos de la unidad coronaria del instituto nacional de cardiología ignacio chávez.

OBJECTIVE: To review the results and complications of thrombolysis in patients with acute myocardial infarction (AMI) and its complications. METHODS: Since june 1989 to august 1994 we studied patients with AMI, who underwent thrombolysis. Clinical characteristics, complications and angiographic results are described. RESULTS: Of the total population 86.3% patients received Streptokinase (SK) and 13.7% recombinant tissue plasminogen activator (rt-PA). In 20 patients the age was under 40 years, 373 between 40-70 years, and 80 patients over 70 years. 84% were men and 16% women. 72% had smoking habit; 21% diabetes mellitus, 43% hypertension, 54% had previous angina and previous AMI in 22%. The location of AMI was anterior in 234 patients and 239 inferior. In 63% enzyme washout was observed, and rapid electrocardiographic evolution in 81%. Postthrombolisis arrhythmias was observed in 64.7%. Major bleeding in 11.8% and central nervous system hemorrhage in 0.4% only with rt-PA. Postinfarction angina in 22%, and re-infarction in 4%. Cardiac rupture in 1.4%, with shock and death. Mitral insufficiency in 2.1% demonstrated by echocardiogram. Coronary angiography was done in 373 patients (80%), of which 50.7% was made in the first 5 days. The culprit artery was anterior descending in 273 patients and right coronary in 95. Left ventricular dysfunction was seen in 23% in patients with anterior AMI, and 5% with inferior AMI. Cardiogenic shock was seen in 7%. Coronary artery bypass grafting was undertaken in 106 patients and coronary angioplasty in 67. The ten days mortality was 8.8%, principally due to cardiogenic shock, ventricular arrhythmias and ventricular rupture. CONCLUSIONS: The usefull permeability in the culprit artery was obtained in 40%, who had coronary angiography done 145 hours posthrombolysis. Mortality was under 10% in this study.

[Analysis of reperfusion by thrombolysis of the artery responsible for acute myocardial infarction]. / Análisis de la permeabilidad por trombolisis de la arteria responsable de infarto miocárdico agudo.

OBJECTIVE: To analyze the role of the culprit coronary artery in myocardial infarction, its evolution and mortality. And to correlate with clinical criteria of reperfussion. MATERIALS AND METHODS: We included patients with clinical diagnosis of acute myocardial infarction (MI) treated with thrombolytic therapy, and coronariography. We used the TIMI study angiographic scale to evaluate the level of permeability of the culprit artery. RESULTS: Of 473 patients with of acute MI; coronariography was made in 377. The most frequent culprit vessel was anterior descending artery in 168 patients (45%) and right coronary artery in 139 patients (36%). In 276 patients the culprit vessel was permeable (73%). Of them in 30 patients, had TIMI 1 alterations, TIMI 2 in 97 patients, had TIMI 3 in 148 patients, only 102 patients had TIMI 0. In anterior MI the most frequent reperfussion arrhythmia was ventricular ectopic beats followed by slow ventricular tachycardia and ventricular tachycardia in 54%, ventricular fibrillation was observed only in six patients, of whom TIMI scale was 2 and 3 in five patients. In inferior MI, ventricular ectopic beats and slow ventricular tachycardia was seen in 25% of patients. In patients with permeable culprit artery we observed significant depression of ST segment, (159 patients, 42%), and significant increase in CK-MB levels, seen in 191 patients (51%). In the group of patients with total occlusion of the culprit artery, twenty-one (30%) had left ventricular disfuntion, and only six of them were in cardiogenic shock. In the group of patients with permeable culprit artery only two percent had cardiogenic shock. Therefore the analysis of the clinical evolution is the maia marker to take into consideration to send patients to early coronary arteriography with the objective to look for other therapeutic alternatives.

[Experimental infarction of the right ventricle. Its natural history]. / Infarto experimental del ventrículo derecho. Su historia natural.

To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 12 dogs in an open chest preparation with intact pericardium. After RVI; mean right auricle pressure and right ventricular end-diastolic pressure (RVEDP) increased (p < 0.05). A statistical significant decline was observed in cardiac output (43%, p < 0.05). However, for left ventricular systolic and end diastolic pressures (LVEDP) a decline was noted only after 120, or 90 min of the production of the RVI. Hemodynamic findings suggested a decreased preload of left chambers, as consequence of ischemic injury of the RV. This feature contributes to low cardiac output. A depression in right and left ventricular function curves were noted after RVI and this condition was maintained after 180 min of experimental observation. Equalized end-ventricular diastolic pressures were noted soon after RVI, a finding that was sustained over the time course of the experiment. Equalization of ventricular filling pressures was noted with RVEDP of < than 10 mmHg and with normals LVEDP. This features do not support, as a main cause, a restrictive role of the pericardium in the genesis of equalized filling pressures in RVI.

[Treatment of acute myocardial infarction with rt-PA in 60 minutes. Cooperative study]. / Tratamiento del infarto agudo del miocardio con rt-PA en 60 minutos. Estudio cooperativo.

UNLABELLED: Thrombolytic therapy (TT) modifies the natural history of acute myocardial infarction (AMI) diminishing morbi-mortality rate. In recent studies, modification of infusion velocity, decreased the mortality 10 percentage points. OBJECTIVE: Test if rt PA administration over an hour is safe and practical. MATERIAL AND METHODS: A prospective, cooperative trial during 3 years, included patients with AMI with less than 6 hours of the onset of symptoms that received rt-PA therapy. Initially 10 mg bolus and then 90 mg over 60 minutes period. Together with the administration of rt-PA, 5000 units of heparin was given, followed by 1000 units per hour adjusted to keep PTT at 1.5 to 2 times normal. All patients received aspirin and according of the evolution adjuvant therapy. We defined bleeding complications and/or cerebrovascular accident related to thrombolytic therapy. RESULTS: We included 225 patients who received rt-PA. Average age was 57.1 +/- 22.2 years, 78.7% males and 21.3% females. Arrival time at hospital was 2.93 +/- 1.7 hours. 82.2% were in class I-II by NYHA. 59.2% had anterior wall location and 32.4% posterior-inferior wall 80% had reperfusion criteria. Only 7.1% required transfusion and 0.4% presented CNS bleeding. The survival rate was 95.2%. The mortality had no relation with bleeding. CONCLUSION: Fast infusion is an effective and safe method. Transfusion requirements are no greater, and CNS bleeding was noted in 0.4% of the cases.

Transesophageal echocardiography and right atrial infarction.

Transesophageal echocardiographic findings in right atrial infarction are described. In three patients with myocardial infarction of one or both ventricles, the association of right atrial myocardial infarction was suspected because of anatomic (two-dimensional) and hemodynamic (Doppler) alterations obtained from transesophageal images. Transesophageal interrogation may prove widely applicable in the evaluation of patients with suspected right atrial infarction.

Effect of hydralazine on vascular mechanics in a canine lobar preparation of pulmonary embolism.

We studied the effect of hydralazine (H) on pulmonary vascular mechanics in an isolated, in situ, canine lobe model of normal and increased pulmonary vascular resistance (Rp) produced by Gelfoam embolization (GE). Pulmonary pressure-flow (P-Q) curves from 24 lobes were obtained at baseline and after each intervention. Hemodynamic parameters for analysis included: the mean critical closing pressure (Ppai), vascular conductance (1/Rp), lobar flow (QL), and the pulmonary inflow pressure (Ppa) at different levels (50, 100, 200, 400, and 600 ml/min) of a fixed flow. After the preparation was stabilized, the 24 lobes were classified into 2 groups. For group 1 (n = 8) we studied the effect of H on the normal pulmonary vasculature. In group 2 (n = 16) we studied the effect of GE. Following GE, this group was further divided in half. For group 2A (n = 8) we followed the natural history of GE with measurements at 15 and 60 min. For group 2B (n = 8) measurements were done 15 min after GE and repeated again 15 min after the infusion of H. For group 1 lobes, H promoted a significant decrease (p less than 0.001) in Ppa at fixed flows of 200, 400, and 600 ml/min compared to baseline, with no change in Ppa for flows below 100 ml/min. QL and 1/Rp increased (p less than 0.01), and there was not any significant change in Ppai. In group 2A lobes, GE produced an increase in Ppa at all levels of flow (p less than 0.01), QL and 1/Rp decreased (p less than 0.05), and there was an increase in Ppai (p less than 0.05). These changes remained stable over the 60 min of observation. For group 2B lobes, GE produced the same hemodynamic changes as in group 2A, and the infusion of H caused a decrease in Ppa at flows between 100 and 300 ml/min. (p less than 0.01) with no change in Ppa at flows below 100 ml/min. QL and 1/Rp increased (p less than 0.01) and Ppai did not change compared to 15 min after GE. We conclude that in the normal canine pulmonary vasculature as well as in the model of GE, H decreased Rp and did not affect mean critical closing pressure, all of which may be explained by an increase in vascular conductance due to an increase in vascular distensibility.

Ventriculoatrial shunts for hydrocephalus and cardiac valvulopathy: an echocardiographic evaluation.

A group of 20 patients with ventriculoatrial shunts placed as surgical treatment for hydrocephalus were evaluated for cardiac lesions, particularly of the tricuspid valve. Patients with histories of septic or thromboembolic events were excluded. In each patient a clinical history, complete physical examination, electrocardiogram, chest x-ray film and M-mode, two-dimensional and pulsed continuous wave and color-coded Doppler echocardiography were performed. Eight patients were found to have cardiac abnormalities including tricuspid valve insufficiency, tricuspid stenosis and insufficiency, and the catheter passing through the foramen ovale into the left atrium. These findings demonstrate that tricuspid valvular lesions are frequent in patients with ventriculoatrial shunts, and that periodic echocardiographic evaluation should be performed routinely.

Behavior of the pulmonary circulation at rest and during exercise in miliary tuberculosis.

We studied the hemodynamic behavior of the pulmonary circulation at rest and during exercise in six patients with MTB. As a group, in contrast to advanced fibrocaseous tuberculosis, these patients exhibited normal pulmonary hemodynamics at rest and during exercise. Only minor abnormalities in pulmonary vascular resistance at exercise (increased PAd-PWP gradient) were noted in two of the patients. The increase in Rp during exercise does not appear to be related to acute hypoxic vasoconstruction but rather to functional changes (compliance or recruitment or both) of the pulmonary microvasculature. In the genesis of these functional changes, chronic alveolar hypoxia and the inflammatory-fibrotic process might be interacting.

[Effect of dopamine on lung vascular mechanics. Its study in the isolated canine lobe model embolized with gel foam]. / Effecto de la dopamina en la mecanica vascular pulmonar. Su estudio en un modelo canino de lobulo aislado embolizado con gelfoam.

After inducing an increase in pulmonary vascular resistance (Rp) in an isolated in situ lobe (LAIS) embolized with gelfoam (GE), the effect of dopamine infused at 12 mcg/kg/min in eight mongrel dogs was evaluated. We studied the rectilinear pressure-flow (QL/PL) relationship, the hemodynamic and blood gas before (condition A), 15 minutes later GE (condition B) and after dopamine infusion (condition C). After GE a decrease in QL and an increase in inflow (PL) and mean critical closing pressures (PLi) were noticed (p less than 0.01). Also decrease in pulmonary vascular conductance (1/Rp) was noted. At condition C a rise in QL and PL were noticed (p less than 0.01), but 1/Rp and PLi did not change. We concluded that dopamine in the LAIS with increased Rp at the used doses does not have vasoactive action for those vessels responsible for the phenomenons where flow resistance or mean critical closing pressure occurs.

[The effect of gelfoam embolism in vascular conduction and critical pressure in the isolated canine lobe]. / Efecto de la embolia con gelfoam en la conductancia vascular y en la presión crítica de cierre en el lóbulo canino aislado.

Pulmonary pressure-flow curves, hemodynamic and blood gas parameters in West's zone II condition were obtained in nine isolated in situ left lower lobes (LLL) before (condition A), and after 15, 30 and 60 minutes of lobar gelfoam embolization (GE) (condition B) in order to know the natural history of this model. After GE a decrease in PaO2 and lobar O2 were noticed (p less than 0.05). Vascular conductance (p less than 0.001) and lobar blood flow decreased (p less than 0.05), accompanied by a significant increase in the inflow (p less than 0.01) and in the mean closing pressures (p less than 0.01). These parameters did not change during the time of observation at condition B. Nor the cardiac output or the minimal closing pressure changed in relation to condition A. LLL angiographic findings showed evidence of arterial occlusion and the pattern of obstruction was not homogeneous. Lobes histology showed occluded arteries of more than 300 micrometers of diameter. We concluded that in this canine model of increased pulmonary vascular resistance, pulmonary vascular conductance and mean closing pressure change, remain stable during 60 minutes after GE allowing us to know the natural history of the preparation. Condition than allow to perform and evaluate other interventions on lung vascular mechanics in the experimental setting of pulmonary embolization.

[Effects of venous segment pressure on the critical closure pressure, in the isolated lung lobe from dogs in situ]. / Efecto de la presión del segmento venoso sobre la presión crítica de cierre, en el lóbulo canino aislado in situ.

In an isolated in situ canine left lower lobe preparation we studied the influence of the distal vascular compartment or venous pressure (PV) on the pressure of arterial vascular segment at zero flow or minimal critical closing pressure (MCCP), while alveolar pressure was held constant and below MCCP. The MCCP-PV curve showed an independent segment when PV was less than 8 mmHg. Above this value (that we define as PV), an slope of 1.08 was found. Our findings indicate that MCCP is not MCCP if PV greater than 8 mmHg (it is MCCP). Because MCCP is higher than alveolar pressure, MCCP must be the back pressure for flow. This finding is not in disagreement with the new concept regarding that MCCP is the back pressure for flow and not alveolar pressure in West's zone II condition.

[Effects of the chest wall and air volume on the perivascular pressure of the arterial segment. Study of the isolated canine lobule]. / Effectos de la pared torácica y del volumen aéreo sobre la presión perivascular del segmento arterial. Estudio en lóbulo canino aislado.

Ten isolated in situ canine left lower lobes (LLL) were studied in West zone II condition. In four dogs (group I) the chest wall surrounding the LLL was surgically removed, in the remaining dogs (group II) this procedure was not done. After basal parameters were obtained, minimal critical pressure (MCCP) was recorded and the influence of increasing alveolar pressure (PA) from o to 20 mmHg was noted. For group I lobes, PA value did not influence MCCP measurements, thus an independent relation between the pressures was found (delta MCCP/delta PA = 0). For group II lobes, when PA less than 6.8 +/- 2.1 mmHg also a delta MCCP/delta PA +/- was noted. Above this PA (PA1) a slope of 0.25 +/- 0.04 was documented for the delta MCCP/delta PA relationship. On the basis of our findings we conclude that MCCP is independent form PA. However if this relationship is studied in the isolated in situ LLL, at open chest with the condition of integrity of the chest wall when PA1 is applied the changes in MCCP are the result of the effect of lung inflation on the chest wall resulting in changes of the extravascular compliance (of the arterial segment) and is not due to a direct influence of PA on MCCP.

[Vascular conductance and critical closing pressure in the isolated canine lung in situ. Its natural history]. / La conductancia vascular y la presión crítica de cierre en el lóbulo canino aislado in situ. Su historia natural.

The vascular pressure-flow relationship (P-QL) in West's zone II condition were studied in isolated, in situ, canine, left lower lobe (ISLL) in order to characterize the total resistance in the pulmonary vascular bed (Rp), the normal values for pulmonary vascular conductance (Cv) and for critical closing pressure (PLc). After the basal parameters were obtained, measurements of Cv and PLc were done every 30' in order to know the natural history (NH) of this canine ISLL preparation. The P-QL relationship of the pulmonary vasculature of the ISLL preparation, perfused under classical zone II conditions, can be characterized by a rectilinear segment at high flow, a curvilinear segment at low flow and a pulmonary arterial pressure that exceeds alveolar (PA) pressure at zero flow. This demonstrates the existence of critical closing pressure (PLc) in the pulmonary vascular bed. The mean control Cv and PLc were 38.5 +/- 14 (ml. min)/mmHg and 7.9 +/- 2.2 mmHg respectively; those parameters did not change through the observation of the experiment. PLc was found to be independent of bronchial flow and it was not related to PA when the values for this pressure were less than 5 cm H20. On the contrary, higher levels of PA pressure were significantly related to PLc (r = 0.94, p less than 0.05). We conclude that in this model of ISLL in West's zone II condition it is possible to study the two components of Rp, one given by vessels that determine changes in flow resistance and for the other vessels disclosing critical closure. The values of these components remained stable over 180' of observation.