[The hemodynamics laboratory: definition and operative characteristics].
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Biomedical subjects
Publications and source records attributed to G Specchia.
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Screening of patients with precordial symptoms is a mayor social problem. Holter monitoring is easy to use because it ambulatory, non invasive, can be repeated without harm, has no contraindications and permits prolonged monitoring. Therefore, it seemed necessary to determine the "role" of this test. We examined all of the Holter monitorings performed in Dynamic electrocardiographic laboratory of the S. Matteo Polyclinic from 1983 to 1986. 480 of the 3365 patients visited, presented precordial symptoms. 162 patients (group A) had established ischemic heart disease (old myocardial infarction and/or coronary arteriography). 318 patients (group B) had no definite diagnosis. 71 subjects from group A and 140 from group B presented a typical symptomatology. Group A showed a 31.48% positivity during the test with 165 ischemic attacks. Group B had 25.15% positivity with 397 ischemic attacks. 51 symptomatic attacks (30%) were recorded for group B. Therefore, there was a mayor incidence of silent ischemic heart disease in both groups. Results obtained comparing Holter monitoring to the bicycle ergometry exercise test and to functional test, were comparable in 56.91% (sensibility 41.71% and specificity 78.62%) in the first case and 61.38% (sensibility 42.50% and sensitivity 73.77%) in the latter. In conclusion, we believe that Holter monitoring is useful in mass screening because it permits monitoring of most ischemic attacks, whether under stress or at rest, symptomatic or silent.
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UNLABELLED: To investigate the incidence of myocarditis, 30 patients, with unexplained congestive heart failure, underwent endomyocardial biopsy. For each case three to five samples were examined on light and electron microscopy. Inflammatory infiltrates and injury to adjacent myocytes consistent with myocarditis were detected in 3 of the 30 cases (10%). Changes attributable to cardiomyopathy were found in the remaining 27 cases. Two of the three patients with biopsy-proven myocarditis were treated with prednisone and azathioprine. Their control biopsies six months later showed interstitial fibrosis and absence of inflammatory infiltrates. They clinically improved but hemodynamic and angiocardiographic patterns failed to show the expected improvement. The third patient affected by myocarditis died two weeks later. IN CONCLUSION: in our series of patients with unexplained congestive heart failure, the incidence of biopsy-proven myocarditis resulted low (10%). The results of the immunosuppressive treatment in two patients with myocarditis were unconclusive. Therefore the effectiveness of such therapy should be confirmed in a larger number of patients.
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Acute lymphoblastic leukemia with hand-mirror cells (ALL-HMC) was diagnosed in a 20-year old patient. Cytochemical investigations revealed a positive reaction for PAS and acid phosphatase. Lymphoid blast cells were studied with various monoclonal antibodies in order to determine their derivation and differentiation. The data obtained (positivity for Leu 9, OKT 11 and OKT 8) suggest that blast cells were of T lineage with OKT 8 phenotype. This report supports the phenotypic heterogeneity of ALL-HMC.
The preliminary results of a prospective study undertaken in patients with a first episode of acute myocardial infarction are presented. The clinical, electrocardiographic and angiographic characteristics of 34 patients who developed early post-infarction angina (group I) were compared with those of 144 patients who remained asymptomatic after the acute infarct (group II). No difference was found between the two groups as to age, sex prevalence, risk factors, presence of stable angina before infarction, severe ventricular arrhythmias or transient congestive heart failure in CCU and peak CK value. Patients of group I had more frequently ecg signs of myocardial infarction in anterior leads (P less than 0.01) than patients of group II. Exercise testing, performed by 23 patients of group I and by 140 patients of group II, was positive in 14 patients with early post-infarction angina and in 37 who remained asymptomatic after the acute infarct (P less than 0.01). The two groups had similar values of left ventricular end diastolic volume index, left ventricular end diastolic pressure and ejection fraction. Patients with early post-infarction angina however had more frequently double or triple vessel disease, while single vessel disease prevailed in group II patients. Although the follow-up period was limited (average 9 months), a higher incidence of cardiac complications was found in group I patients (P less than 0.01). These data show that early post-infarction angina defines a high-risk subset of patients among those with recent myocardial infarction. A more aggressive approach, including thrombolytic therapy and coronary angioplasty, seems warranted.
This study was designed to assess, by two-dimensional echocardiography, the effects of anticoagulant therapy on left ventricular thrombosis detected after acute myocardial infarction. Thirty-eight patients with left ventricular thrombi detected by two-dimensional echocardiology within 5 weeks (mean 4) of the onset of infarction were randomly assigned to the following groups: group A consisted of 19 patients who received oral anticoagulants (acenocoumarin 1-6 mg daily regulated to keep prothrombin time within the range of 25 to 35%) and group B which consisted of 19 non-treated control patients. Seventeen patients from both groups were restudied 15 days, 3 months and one year later to evaluate the changes in size of thrombi. Echocardiographic examinations were read blindly; a significant decrease in ventricular thrombus size was taken as a greater than or equal to 5 mm reduction of thickness in the apical views. In Group A, 9 patients showed a complete resolution of thrombus at the 15 day study; at one year, thrombus had resolved in 15 and persisted unchanged in size in 2 patients. The mean dimension of thrombi in patients of group A was 18 +/- 6.6 mm at the screening examination and decreased to 6.6 mm, 3.8 mm and 2.2 mm, respectively, at 15 days, 3 months and one year follow-up studies. Among 17 patients of group B at the 15 day study, two had resolution of thrombus and 15 were unchanged; at the one year examination thrombus was resolved in 4, decreased in size in 4 and persisted unchanged in 9 patients. Analysis of variance of the dimensional changes of thrombi in the two groups of patients confirmed a significant efficacy of anticoagulant therapy (P less than 0.001). On the basis of our results we conclude that full-dose anticoagulant therapy, started early (within 5 weeks) after acute myocardial infarction, is effective in the resolution of left ventricular thrombosis.
Out of 3,900 patients who performed an exercise test at our clinic, 3 patients demonstrated a walk-through phenomenon (WTP), defined as the occurrence of mild angina during the first stages of exercise with disappearance of chest pain at higher workloads despite a greater pressure-rate product. 2 patients had variant angina, one with normal coronary arteries and the other with single vessel disease, while the third patient had stable exertional angina and a severe coronary artery disease with occlusion of two major vessels retrogradely filled by collateral channels. Repeat exercise tests failed to reproduce constantly the WTP in the 2 patients with variant angina, while in the third patient the phenomenon was repeatedly induced by exercise testing. Thus the WTP, although rarely found during exercise testing, can be observed in two subsets of patients. In variant angina the WTP is not reproducible and is probably due to coronary spasm, spontaneously subsiding during exercise. In patients with exertional angina and severe coronary artery disease, the WTP can be repeatedly observed during exercise and is likely to be secondary to a delayed vasodilation of collateral vessels. The clinical characteristics of the patients and the response to repeat exercise tests may be useful in identifying the different pathogenetic mechanisms.
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30 patients with a previous myocardial infarction who had undergone diagnostic conventional left ventriculography and coronary arteriography had left ventriculography also performed by digital subtraction angiography after intravenous injection of contrast medium; the mean interval between the two investigations was 2.3 days. The conventional and the digital subtracted left ventricular images were computer-processed; global ejection fraction (obtained by the volumes calculated with the Dodge method) and segmental wall motion (from a quantitative analysis performed according to the Stanford method) were compared. We found a close correlation for the ejection fraction obtained by the two techniques (r = 0.89, p less than 0.01); absolute values proved to be slightly higher in the digital subtraction angiography. Segmental wall motion was significantly correlated too (p less than 0.05 for all the segments of the ventricular silhouette but for the one corresponding to the base of the heart). Digital intravenous angiography provides an accurate and less invasive method to evaluate left ventricular function.
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Exercise may induce ventricular arrhythmias (VA) in patients with coronary artery disease. Exercise-induced VA can identify a subset of patients at higher risk of cardiac sudden death. The role of myocardial ischaemia and/or left ventricular disease in the appearance of VA during exercise is not completely understood. The incidence of VA during exercise-induced myocardial ischaemia was investigated in patients with suspected CAD or those undergoing a stress exercise test after a previous myocardial infarction (MI). Patients were divided in four groups. Group A, 836 patients without a previous MI showing exercise-induced myocardial ischaemia associated with ST-segment depression--group B, 72 patients without a previous MI and exercise-induced ST-segment elevation--group C, 50 patients survivors of a recent (1 month) MI and exercise-induced ST-segment depression--group D, 580 patients with an old MI (greater than 3 months) and a positive exercise test associated with ST-segment depression. Exercise-induced VA were found to be significantly more frequent in patients of groups C (40.0%) and B (23.6%) as compared with groups A (5.1%) and D (7.06%) (P less than 0.001). Furthermore VA in groups B and C were more frequently complex (couplets, triplets, ventricular tachycardia and fibrillation). In all groups the appearance of VA during exercise-induced myocardial ischaemia did not appear to be related to exercise duration, maximal heart rate, maximal work capacity, left ventricular end diastolic pressure, ejection fraction or extent of coronary artery lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
Measurement of coronary sinus blood flow by continuous thermodilution is a well established technique for the clinical study of myocardial perfusion. More recently, advances in catheter technology enabled regional left ventricular flow measurements. In particular, measurement of flow from the great cardiac vein appears to accurately reflect the perfusion of the left anterior descending coronary artery. This regional approach allowing the correlation with coronary arterial anatomy, has contributed to an improved understanding of the mechanisms by which functional factors interact with organic narrowing in the genesis of myocardial ischemia at rest, during provocative tests and during exercise. In addition, it has provided useful information in the evaluation of antianginal drugs through the discrimination between the effects on coronary resistance and myocardial oxygen consumption.
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To assess if cold-induced vasoconstriction may persist during exercise and contribute to the development of myocardial ischaemia, we studied 11 patients with exertional angina and angiographically proven coronary artery disease, in all cases involving the proximal portion of the left anterior descending artery. Great cardiac vein flow (GCVF) was measured by the thermodilution technique and the coronary resistance of the abnormally perfused anterior region (ARCR) was calculated as the quotient of mean arterial pressure and GCVF. All patients performed a supine bicycle exercise test (ET1) until angina occurred. After recovery, they underwent a cold pressor test (CPT) and then performed a second exercise test (ET2) while cold stimulation was continued. During ET1, ARCR decreased (from 1.53 +/- 0.43 to 1.04 +/- 0.35 mmHg ml-1 min-1, P less than 0.001) as a result of the metabolic vasodilation, while it rose, although non significantly, during CPT despite the increase in double product (P less than 0.001), reflecting the augmented myocardial oxygen consumption. However, such abnormal response to CPT did not persist during ET2, because ARCR decreased to a value non significantly different from that achieved at peak ET1. In five patients, who showed a reduced exercise tolerance during ET2, ARCR dropped by 22% during ET2 compared with 34% decrease during ET1. However, such a difference was unlikely to account for the reduction in exercise tolerance, because the double product at peak ET2 was never lower than the corresponding value at peak ET1. Our data show that the inappropriate vasoconstriction induced by CPT in an abnormally perfused myocardial region does not persist during exercise, when metabolic vasodilation occurs.(ABSTRACT TRUNCATED AT 250 WORDS)
Regional myocardial blood flow during exercise was determined using the thermodilution technique in 2 patients suffering from both spontaneous and exertional chest pain. In both cases we observed that effort-related anginal attacks were due to coronary spasm with sudden reduction of regional left ventricular blood flow. In 1 patient the exercise-induced ST-segment elevation in the anterior leads was accompanied by a reduction of flow in the great cardiac vein. In the second patient the exercise-induced ST-segment depression in the lateral leads was accompanied by a reduction of coronary flow in the area supplied by the circumflex artery. In 1 patient, nifedipine was effective in prolonging exercise tolerance by preventing the occurrence of coronary spasm and by increasing blood supply to the ischemic region during exercise.