Combined bilateral abdominal hernia repair and peritoneal catheter insertion.
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Biomedical subjects
Publications and source records attributed to E Coppola.
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Fibrinolytic therapy is a major advance in the treatment of coronary artery disease. A marked elevation in plasma and urinary metabolites of thromboxane A2 (TXA2) after administration of thrombolytic therapy has been observed and has been related to a direct effect of thrombolytic drugs on platelets. To test this hypothesis we evaluated the 11-dehydro-thromboxane B2 (11-d-TXB2) level, as an index of platelet activation, in 20 healthy subjects and in 30 patients with acute myocardial infarction (AMI). Patients with infarction received streptokinase (n = 8), recombinant tissue-type plasminogen activator (rt-PA) (n = 8), or thrombolytic therapy preceded by acetylsalicylic acid (n = 7) or were treated without thrombolytic therapy (n = 7). The urinary 11-d-TXB2 level in healthy control subjects was 327 +/- 126 pg/mg creatinine. A significant increase was observed in patients with AMI with no difference between those who received no thrombolytic therapy (673 +/- 283 pg/mg creatinine in the first 12 hours) and those who received streptokinase (833 +/- 613 pg/mg creatinine) or rt-PA (836 +/- 653 pg/mg creatinine). Patients pretreated with acetylsalicylic acid had urinary 11-d-TXB2 values ranging between 361 and 155 pg/mg creatinine. A significant difference in 11-d-TXB2 values was observed only when patients who were reperfused were separated from those who remained occluded according to angiographic criteria (1085 +/- 498 vs 391 +/- 227 pg/mg creatinine in the first 12 hours, p less than 0.001). We conclude that reperfusion and not thrombolytic agents per se appears to be the factor that induces platelet activation and consequently facilitates reocclusion.
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Fifty-four patients with acute myocardial infarction were treated with thrombolytic therapy (27 with rTPA and 27 with streptokinase). In all the subjects CK was monitored (every 3 hours) and ergometric test, echocardiogram, and 24 hours holter ecg were performed in the pre-discharge period. In 22 of the patients, coronary angiography was also performed. No differences were shown between the two groups of patients as regards CK values and ejection fraction. Repetitive ventricular premature beats were registered without difference between the two groups (23% in patients treated with SK and 18% in the patients treated with rTPA). No bleeding events were shown in the patients treated with rTPA without calciparin. On the other hand no difference there was between patients treated with rTPA + calciparin and patients treated with SK with or without calciparin.
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Circadian rhythms have been described both for acute myocardial infarction (AMI) and sudden death. In this study the diurnal distribution of ventricular tachycardia (VT) in patients with AMI was analyzed. Ninety-four AMI patients with greater than or equal to 1 VT on Holter electrocardiographic monitoring who were not taking antiarrhythmic drugs were studied. Forty-seven patients had a recent AMI (group A) and 47 an old AMI (group B). Chronobiologic analysis was made by single cosinor method. There were 157 VTs (mean 1.67 VTs/patient, range 1 to 10) in the 94 patients: 70 in group A and 87 in group B. A significant circadian rhythm of VT was found in the total population with acrophase at 2:29 P.M. The hourly distribution of VT showed a tendency to bimodality, which seemed due to a different time of peak VT occurrence in group A (significant rhythm with acrophase at 4:40 P.M.) and group B (significant rhythm with acrophase at 12:39 P.M.). Thus, the hourly VT frequency in patients with AMI has a significant circadian variation with the highest occurrence in the awake hours, similar to the rhythms described for AMI and sudden death.
A 24-hr electrocardiographic monitoring was performed in 406 patients (297 with ischemic heart disease). Forty-one episodes of ventricular tachycardia were detected in 32 subjects (7.88%). The average rate of tachycardia was 127.4 (range 180-65). No correlation was observed between the rate of ventricular tachycardia and the heart rate 30, 20, and 10 min before and at the moment of the episode. A circadian rhythm of all the episodes was demonstrated, with an acrophase at 1102 hr. A different acrophase was observed for the QT interval. No significant rhythm was observed for premature ventricular beats in the patients with ventricular tachycardia. The circadian variation of tachycardia suggests that this arrhythmia is related to sympathetic tone, but it will require further studies with a larger number of patients with ventricular tachycardia to clarify this problem.
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Thirteen asymptomatic adults less than 40 years old who showed tall right precordial R waves on the ECG were examined by VCG, M-mode and two-dimensional echocardiography (2D Echo). Common causes of QRS anterior displacement, such as right ventricular enlargement or right bundle branch block, were excluded in each subject. Although each subject was normal at physical examination, 2D Echo revealed areas of left ventricular hypertrophy in eight of these 13 subjects. Four had a prevailing hypertrophy of the basal portion of the interventricular septum, three had an isolated apical hypertrophy, and one had a diffuse concentric left ventricular hypertrophy. Results were normal in five cases. 2D Echo classification was confirmed by heart catheterization findings, when available. The subjects with asymmetric septal hypertrophy showed low-voltage QRS leftward forces on the ECG and VCG. ECGs and VCGs were not useful in differentiating the subjects with atypically distributed left ventricular hypertrophy from the normals: high-voltage QRS leftward forces and T wave abnormalities were evident in some subjects of both groups. Tall right precordial R waves may constitute a marker of hypertrophic cardiomyopathy in asymptomatic young adults. 2D Echo is useful to exactly classify these subjects.
Left atrial dimensions were measured using cross sectional echocardiography in 37 patients with mitral valve disease and 30 normal subjects of similar ages. The anteroposterior (AP), superior-inferior (SI), and medial-lateral (ML) left atrial dimensions were determined at the end of ventricular systole using parasternal long and short axis and apical four chamber views (for SIa and MLa). To assess the reliability of these measurements cross sectional echocardiographic and angiographic left atrial volumes were compared in 19 patients with mitral valve disease, giving an excellent correlation. A moderate correlation was found between the anteroposterior dimension of the left atrium obtained using M mode echocardiography and that obtained using the parasternal short axis and long axis projections. In normal subjects a good correlation was found between SI and ML dimensions, while a lower correlation was found between SI and AP, and ML and AP dimensions. The SI dimension was the major axis of the left atrium and AP dimension the minor axis. In patients with mitral valve disease a good correlation was found between SI and ML dimensions, while SI and ML dimensions had a low correlation with AP dimensions. The AP dimension was the minor axis of the left atrium, while the SI and ML dimensions were not significantly different. All left atrial dimensions were significantly greater in patients with mitral valve disease than in normal subjects. Of 30 patients with at least one dimension increased, all three dimensions were abnormal in 16, two dimensions were increased in 10, and only one dimension was increased in four. AP, SI, and ML dimensions were abnormal in 25, 20, and 27 patients, respectively. Cross sectional echocardiography may provide a reliable estimate of left atrial dimensions. In patients with mitral valve disease a thorough examination of the left atrium using multiple cross sectional views is necessary to detect asymmetric left atrial enlargement and to measure the degree of left atrial dilatation.
The electrocardiographic and echocardiographic (M-mode) data were analyzed in 29 patients affected by mitral or combined mitral and aortic valve disease and with hemodynamically documented biventricular overload. No electrocardiographic parameter significantly correlated with the left ventricular internal dimension at end diastole (LVIDd), the left posterior wall (LVPW) thickness and the left ventricular mass (LV mass). A significant correlation was observed between the R/S ratio in V1 and V2, the rV1 and either the end-diastolic right ventricular internal dimension (RVIDs) or the pulmonary artery systolic pressure (PASP). The R/S ratio greater than or equal to 1 in V1 was the most sensitive among the conventional electrocardiographic criteria of right ventricular enlargement. Three groups of patients were selected on the basis of RVIDd and LV mass: Group A included nine patients with right ventricular dilatation and normal LV mass; Group B included ten patients without right ventricular dilatation and with increased LV mass; Group C included ten patients without right ventricular dilatation and with normal LV mass. The R/S ratio in V1 was significantly greater in patients in group A than in those in groups B or C. No electrocardiographic parameter was found to be significantly different between groups B and C. When only LV mass was considered (independently from RVId and PASP), no electrocardiographic parameter differentiated patients with LV mass greater than 203 g from those with LV mass less than 203 g. We conclude that in patients with biventricular overload secondary to acquired valvular disease: 1) the electrocardiographic diagnosis of left ventricular enlargement is unreliable; and 2) the R/S ratio in V1 is the most sensitive parameter to predict right ventricular enlargement or severe pulmonary hypertension.
The electrocardiographic and vectorcardiographic (Frank system) features of the first degree relatives of subjects with documented familial hypertrophic cardiomyopathy were analysed. A total of nine affected members and 29 relatives were examined in four families. THe subjects were considered to be affected when the septal to free posterior wall thickness ratio exceeded 1.3 at M-mode echocardiography. Four relatives had asymmetric septal hypertrophy. Among 25 relatives without evidence of asymmetric septal hypertrophy, two over 20 years and 10 under 20 years of age showed increased voltage of QRS anterior forces (Qz amplitude greater than 0.80 mV) on the orthogonal electrocardiogram. The vectorcardiographic data of the relatives under 20 years of age without evidence of asymmetric septal hypertrophy (18 subjects) were compared with those of 38 normal control subjects of comparable age range. The young relatives without disproportionate septal hypertrophy had significantly greater Qz amplitude and Q/Rz ratio than the normal control subjects. In contrast, the echocardiographic data were not significantly different. We suggest that the electrocardiographic finding of abnormal anterior forces in one or more first degree relatives of subjects with documented hypertrophic cardiomyopathy may constitute a valuable aid in ascertaining the genetic transmission of the disease and in recognising affected members without echocardiographic evidence of hypertrophic cardiomyopathy.
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