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The effects of oral administration of guaiacolic ester of acetyl salicilic acid in 24 patients with chronic obstructive lung disease have been evaluated. 1.5 g of this drug were given daily into 3 administrations improving both objective and subjective symptomatology in 19 of the 24 patients after 1 or 3 weeks of treatment. Moreover, a statistically significant improvement of FEV 1" (p less than 0.001), Raw (p less than 0.005) and FEV 1"/VC (p less than 0.01) was observed. The remaining 5 patients discontinued the treatment failing the improvement of the subjective symptomatology.

The effectiveness of chronic treatment with nifedipine in patients (pts) with a history of stable angina on effort has been evaluated in a double-blind study in 15 subjects of both sexes, aged 45 to 65 years. All pts underwent diagnostic cardiac catheterization and selective coronary angiography, which showed stenosis of one or two main coronary vessels between 50 and 70%. The pts, after 2 weeks of observation, underwent erect bicycle exercise test with increasing workloads. After 4 weeks of treatment with nifedipine or placebo the stress test was repeated. Nifedipine treatment reduced the weekly number of anginal attacks as well as the weekly number of nitroglycerin tablets consumed by the pts, increased maximum workload tolerated and reduced the S-T segment depression for the same workload, meanwhile heart rate and blood pressure did not change significantly either at rest or during exercise. The result of this study indicate that nifedipine is useful in the treatment of pts with stable angina on effort.

The Authors studied correlations between angiocardiography and changes of R wave amplitude (delta R) during effort in 113 patients. They showed coronarographic evidence: 69 with stenosis greater than or equal to 70% of at least one major coronary vessel and 44 with no significant lesions. delta R values greater or equal than 0 were considered as pathologic. delta R appeared greater than or equal to 0 in 8 of 14 patients (57%) with single stenosis, 4 (28%) with abnormal wall motion (AWM). delta R increase or unchanged in 26 of 31 (84%) patients with double stenoses, 25 of them (81%) with AWM. delta R was greater than or equal to 0 in 22 of 24 (92%) with triple stenoses. In subjects with milk coronary artery disease (CAD) R wave increased or unchanged in 47% (19/44). Pathologic changes of R wave are highly frequent in CAD patients, especially in those with severe impairment. These changes, however, are not specific or costant because they appeared enough frequently in subjects with normal doronary vessels, and, moreover, R wave may decrease also in CAD patients with severe impairment. The Authors consider that evidence of delta R values greater than or equal to 0 may not be considered as a sign of CAD, but it must be evaluated with the other data showed by ergometric tests.

We evaluated the protective effect of Diltiazem from pacing-induced myocardial ischemia in 9 patients (pts) with coronary heart disease (CAD) and stable effort angina by studying the changes in systemic and coronary hemodynamics during pacing. Hemodynamic parameters were evaluated at baseline and at peak pacing before and after Diltiazem, 25 mg i.v. Diltiazem prevented angina in 6 of 7 pts who presented angina in the control pacing. This beneficial effect was accompanied at peak pacing rate by a significant fall in ST depression, arterial pressure, rate-pressure product and left ventricular (LV) end-diastolic pressure, while no significant changes were observed in LV dp/dt max, coronary blood flow and coronary vascular resistance. Therefore, Diltiazem exerts a protective effect from pacing-induced myocardial ischemia in pts with CAD and stable effort angina, without impairing LV function. This beneficial effect is due to a reduction in myocardial metabolic requirements, rather than to an improvement of blood supply to the ischemic myocardium.

The correlation between R wave voltage variations (delta R) and the angiographic severity of coronary artery disease (CAD) at progressively increasing heart rate (HR) steps was evaluated in 51 patients (pts) without CAD (OV), in 42 pts with single (SVD), in 43 with double (DVD) and in 59 pts with triple vessel disease (TVD). At the end of stress the sensitivity of delta R was higher in DVD and TVD pts than in SVD pts. There was no clear correlation between exercise-induced R wave changes and the angiographic severity of CAD, since the qualitative and quantitative delta R evaluation during effort showed similar changes in delta R for a wide range of HR's in the entire study population. Since different degrees of exercise tolerance were found in pts with SVD, DVD and TVD, we hypothesize that the correlation between delta R and the severity of CAD at the end of stress testing may be artifactual.

Exercise-induced changes of R wave amplitude (delta R) during exercise has been employed to improve the reliability of stress testing in detecting patients with coronary artery disease. Several authors postulated that delta R are related to changes of ventricular volumes. Furthermore Valsalva Maneuver (VM) is able to induce a decrease of left ventricular volumes induced by VM and the variations of R wave. Echocardiographic method was used to determine left ventricular volumes and R wave amplitude changes were evaluated by Frank's lead. Our findings suggest that R wave amplitude changes are not related to variations of cardiac volume. Electrophysiological mechanisms of delta R need further investigation.

The incidence of ventricular arrhythmias observed during exercise (EVA) was correlated with the presence of previous myocardial infarction (IM) and angiographic severity of coronary artery disease (CAD) in 162 patients (pts.) with stable angina on effort, who had a positive stress test and greater than 70% stenosis of a major coronary artery. Our study population was divided in two groups: the first was composed of 95 pts. with previous MI, the second of 67 pts. without previous MI. Pts. of both groups were subdivided according to severity of CAD and to presence and degree of abnormal segmental wall motion (ASWM). In the MI group only 11.5% of pts. had single vessel disease, and 86.3% had ASWM. In pts. without MI 28.6% had single vessel disease; ASWM was found in 59.7% (p less than 0.001 vs MI pts.). Pts. with MI showed a higher incidence of EVA than pts. without MI (60% vs 32.8%, p less than 0.001). In both groups EVA were more frequent among pts. with double, triple vessel and main left CAD, than in pts with single vessel disease, but the difference was not significant. In general, EVA were found to correlate better with the number of areas with ASWM: in both groups significant differences of EVA frequency were found when pts. with normal left ventricular function were compared to those with more severe ASWM, while no difference was found between pts with and without MI who had the same degree of CAD. The most severe EVA (Tilkian's classification), were found in pts with a previous MI and a high ASWM score. In conclusion, our results show that a previous MI affects the development of EVA in pts. with stable effort angina. However EVA seem to be better correlated with the severity of LV impairment than with the extent of CAD.

Our study evaluated the effects of verapamil in elderly patients with stable effort angina using a medium-term double-blind placebo-controlled protocol. Thirty-nine consecutive patients, 23 middle-age patients (50 +/- 6 years; range 38-60 years) and 16 elderly patients (66 +/- 2 years; range 65-70 years) with exertional angina were chosen. After a run-in period, both groups received treatment with either placebo or verapamil--360 mg daily--for 4 weeks. During treatment, weekly angina frequency and nitroglycerin consumption were significantly reduced in both groups. Verapamil significantly decreased the rate-pressure product at rest in elderly patients and in both groups at submaximal exercise, due to a reduction in heart rate in both groups and to a more marked decrease in arterial pressure in older patients. At peak exercise, the rate-pressure product was unchanged in both groups after verapamil, while exercise capacity showed a significant improvement in the middle-aged, and ST segment depression was reduced in both groups. After verapamil, 30% of middle-aged patients and 44% of elderly patients had to stop exercising because of angina. Side effects were rare and no drop-out was recorded. Verapamil exerted its antianginal action by means of a decrease in myocardial oxygen consumption at rest and at submaximal exercise in the elderly, while only at submaximal exercise in the middle-aged. Therefore verapamil at the dose of 360 mg daily proved an effective antianginal drug with a safe effect profile also in elderly patients.

A multicenter, double-blind, randomized, placebo-controlled trial was conducted to assess the effects of verapamil on total mortality, cardiac mortality, reinfarction, and angina after an acute myocardial infarction. All patients, aged 30 to 75 years, consecutively admitted for acute myocardial infarction between 1985 and 1987 to the participating centers, and without contraindications to verapamil or history of severe heart failure were enrolled. Seven to 21 days (mean 13.8) after myocardial infarction, 531 patients were randomized to verapamil retard 360 mg/day, and 542 patients to placebo. At baseline, the 2 groups of patients had similar characteristics. Mean age was 55.5 years and 91% were men. During a mean follow-up of 23.5 months, 5.5% of the patients died. No differences between verapamil and placebo were observed in total mortality (n = 30 and 29, respectively) and cardiac death (n = 21 and 22, respectively). The verapamil group had nonsignificant lower reinfarction rates (n =39 vs 49). The number of patients developing angina was significantly less in the verapamil group (n = 100 vs 132, RR = 0.8, 95% confidence interval 0.5 to 0.9). There were no differences in discontinuation of therapy caused by adverse reactions. This trial showed no effect of verapamil on mortality. The lower reinfarction rates found in the verapamil group are in agreement with the results of other studies.

Lo studio parte dalla constatazione dell'imponente numero di pubblicazioni ad argomento catastrofico che si realizzarono nel Regno di Napoli a partire dal 1631 della grande eruzione vesuviana e per tutto il s. XVII lungo il quale si moltiplicarono i fenomeni tellurici e le emergenze politico-sanitarie. Relazioni cronachistiche, trattati scientifici, opere di carattere devozionale, riflessioni filosofico-morali, ma anche un'importante quantità di testi poetici affollano i banchi delle librerie per contribuire all'interpretazione di una serie di eventi che stravolgevano le consuetudini quotidiane costringendo la popolazione a confrontarsi con quel che l'antropologo Ernesto de Martino avrebbe poi chiamato la "crisi della presenza". Nel fronteggiare lo choc cognitivo tipico di ogni grande fenomeno distruttivo, questa produzione, e soprattutto quella più francamente letteraria e poetica, provvedeva a riconfigurare il sistema culturale cittadino, fornendo anche una diversa interpretazione del sistema urbano, i cui assi venivano rovesciati da Ovest (originario polo mitologico in virtù dell'estensione cumana e delle memorie virgiliane) a Est (dove invece si erge il vulcano, che diviene il nuovo centro di una mitologia tellurica e ctonia apparentata a quella etnèa), e riconfigurata secondo le coordinate verticali basso/alto (giù ci sono in conflitti, la morte, le potenze della distruzione, su ci sono i santi e i condottieri che proteggono). Inserendosi nell'ambito della ricerca ERC "Discopose", il contributo mira a fornire una lettura della produzione letteraria napoletana del s. XVII che reinterpreti le coordinate di stile (il marinismo e la cultura barocca) all'interno di un sistema tipologico-culturale coerente che abbraccia insieme rappresentazione cartografica, illustrazione pittorica, cultural scientifica e linguaggio della poesia.

Si prende in esame la descrizione e la narrazione di terremoti ed eruzioni vulcaniche in testi dell'età moderna. Viene quindi discussa la funzione delle narrazioni come garanzia di continuità della vita e dell’ordine sociale. Segue la disamina del lessico dei disastri e l’esame dei nomi del terremoto.

To evaluate whether histamine exerts a direct effect on coronary hemodynamics in humans, and to investigate the role played by H1and H2receptors in this response, intracoronary saline solution or histamine (4 μg) was administered in 10 patients with normal coronary arteries during diagnostic cardiac catheterization. Histamine injection was repeated after intravenous Cimetidine (400 mg) and diphenhydramine (10 mg). The electrocardiogram, arterial pressure and thermodilution coronary blood flow were continuously monitored during and for 40 seconds after each injection.Immediately after histamine injection there was a significant increase in coronary blood flow (65 ± 6%) and a decrease in coronary vascular resistance ( − 40 ± 3%) (both p < 0.001), with minor changes in the RR interval and the mean arterial pressure. H2receptor blockade with Cimetidine did not affect these changes, while H1receptor blockade with diphenhydramine sig- nificantly reduced the histamine-induced increase in coronary blood flow and the decrease in coronary vascular resistance (26 ± 6%, p < 0.005 and −18 ± 5%, p < 0.001, respectively). Twenty to 30 seconds after histamine injection, a significant decrease in mean arterial pressure (−17 ± 2%, p < 0.001) and in the RR interval (−4 ± 1%, p < 0.01) was observed. These changes persisted after H2receptor blockade with Cimetidine, but were completely abolished after H1receptor blockade with diphenhydramine. In each case coronary and systemic hemodynamics returned to normal within 40 seconds of the injection.Therefore, in patients with normal coronary arteries, histamine induces a direct dilation of the small resistance coronary arteries, regardless of myocardial metabolic requirement, that is predominantly, but not completely, mediated by H1receptors.

Histamine is widely present in human tissues and can be released by immunologic and nonimmunologic reactions. Although several direct cardiovascular effects of histamine have been demonstrated in humans, little is known about the direct effects of histamine on the human coronary circulation in vivo. Therefore, we investigated the changes in coronary hemodynamics induced by bolus intracoronary administration of 4 micrograms of histamine to 11 patients with angiographically normal coronary arteries under continuous monitoring of R-R interval from the electrocardiogram, arterial pressure (AP), and coronary sinus blood flow (CBF), measured by thermodilution. Immediately after the end of the intracoronary histamine bolus, with R-R interval and AP unchanged, CBF increased from 144 +/- 20 to 238 +/- 27 ml/min (p less than 0.01) and coronary vascular resistance decreased from 0.7 +/- 0.16 to 0.42 +/- 0.1 mm Hg/ml/min (p less than 0.01). No change in coronary hemodynamics was observed after bolus intracoronary administration of physiologic saline. The effects of histamine on systemic hemodynamics consisted of a transient fall in AP and R-R interval, starting after the onset of changes in coronary hemodynamics. These data show that histamine possesses a direct coronary vasodilator effect in humans, independent of the determinants of myocardial oxygen consumption.

It has been previously reported that at treadmill exercise testing an abnormal ratio of recovery systolic blood pressure (SBP) to peak exercise SBP is more sensitive than exercise-induced angina or ST segment depression for diagnosing coronary artery disease (CAD). To investigate whether the SBP ratio keeps its diagnostic value during upright bicycle exercise, we evaluated the ratio of postexercise SBP to peak SBP in 73 patients with angiographically documented CAD and in 48 patients with normal coronary arteries (OV group) undergoing maximal stress testing on a bicycle ergometer. Three minutes after exercise ended, SBP ratio was significantly higher in the CAD than in the OV group (0.79 +/- 0.1 vs 0.71 +/- 0.08; p less than .001). Setting the upper normal limits of the recovery SBP ratio at 2 SDs from the mean for the OV group (SBP ratio = 0.98 and 0.88 at 1 and 3 min after exercise, respectively), with an increase or no change in SBP ratio at between 1 and 3 min of recovery considered an abnormal response, the sensitivity of SBP ratio was 30%, the specificity was 83%, and the accuracy was 51%. The respective values for ST depression were 81% (p less than .0001 vs SBP ratio), 48% (p less than .001 vs SBP ratio), and 67% (p less than .01 vs SBP ratio). Thus, for bicycle ergometer exercise testing, ST segment depression seems to be more accurate than SBP ratio in diagnosing CAD.

The effect of increased potassium conductance on the genesis of R-wave amplitude increase during acute myocardial ischemia has been studied in the isolated perfused rat heart by simultaneously recording the R-wave amplitude of epicardial electrograms (VEE), heart rate (HR), coronary flow rate (CFR), left ventricular diastolic pressure (LVDP), and left ventricular systolic pressure (LVSP). The experiments were performed during basal and partial or total ischemic conditions at spontaneous or fixed HR. In some experiments, potassium conductance was increased by means of high-calcium (8 mM) or acetylcholine chloride (10−6 M) perfusion. In the control experiments, partial ischemic perfusion produced an increase in VEE and LVDP and a decrease in HR, CFR, and LVSP; total ischemic perfusion exaggerated these variations. High-calcium perfusion provoked an increase in VEE and LVDP and a decrease in HR, CFR, and LVSP during basal conditions (p

Ventricular arrhythmias are the most common cause of death among patients with coronary artery disease; this is more evident in the elderly, who tend to have more severe coronary artery disease and age-dependent modifications of cardiac electrophysiology. Lysophosphoglycerides, which accumulate in the ischemic myocardium, are responsible for oscillatory after-potentials and may contribute to the development of ventricular arrhythmias. The aim of this study was to examine the effects of lysophosphatidylcholine (5 x 10(-5) M) in the absence or presence of epinephrine (10(-6) M) in isolated, perfused hearts from adult (6-12 months old) and senescent (24 months old) rats. Rat hearts (30/group) were randomly divided into four groups each of which included hearts of 6, 12 and 24-month old rats. The groups comprised a control group, a group treated with epinephrine, a group treated with lysophosphatidylcholine and a group treated with both epinephrine and lysophosphatidylcholine. Analysis of arrhythmias indicated a linear correlation between epinephrine- and lysophosphatidylcholine-induced ventricular arrhythmias and age. The incidence of arrhythmias was higher in the hearts treated with epinephrine and lysophosphatidylcholine together than in those treated with either substance separately (p less than 0.01). The results indicate that age influences the arrhythmogenic action of lysophosphatidylcholine, and that epinephrine contributes to this effect.

Objective: The contractile response to digitalis and β adrenoceptor agonists is lower in the senescent than in the adult myocardium, while the development of ventricular arrhythmias is increased. The aim of this study was to examine the effects of aging on cardiac response to digitalis and an adrenergic agonist used clinically. Methods: The electrical and mechanical responses were tested in isolated and perfused hearts from 3-24 month old rats receiving 15 min infusion of digitalis drug (ouabain, 6 × 10−5 M) alone, and after 5 min of β adrenoceptor agonist drug (epinine, 1.5 × 10−7 M). Results: Ouabain action was associated with a rise in left ventricular end diastolic pressure (p

To evaluate and quantify the relationship between premature ventricular contractions (PVCs) and heart rate (HR), 57 patients (48 men and 8 women, mean age 59.8 ± 7.9 years) with severe PVCs (Lown-Wolf grade ≥3a) over 24 hours of Holter monitoring were studied. Twenty had no coronary artery disease (CAD), 25 had angiographically documented CAD, and 12 had acute myocardial infarction. All parameters of the 24-hour recordings from two ECG leads were measured by a Holter analyzer designed in our laboratory, based on fast microprocessors and controlled by a microcomputer. Scatter diagrams of the number of PVCs per minute as a function of HR and correlation coefficient were computed for various HR values corresponding to a total number of minutes greater than five. A positive correlation ( r ≥ 0.35) was found in most patients without CAD (85%); there was a complex relationship between the strength of the correlation and the presence of CAD or acute myocardial infarction because of a greater variability in the results of correlation coefficient analysis (coefficient of variation 62%, 208%, and 145% in patients without CAD, with CAD, and with acute myocardial infarction, respectively). The incidence of a positive correlation was similar in patients with Lown-Wolf grade III (63%), IVa (82%), or ≥IVb (67%) arrhythmias. The reproducibility of the correlation coefficient of the relationship between PVC frequency and HR was tested in 15 patients. The mean value of the correlation coefficient was 0.801 ± 0.169 for the first test and 0.805 ± 0.22 ( p = NS) for the second test. Results of our study show a positive correlation between PVCs and HR in patients without CAD but not in those with CAD or acute myocardial infarction. This is because of a greater variability in coefficient of correlation analysis in the latter patients, even though our mathematical model shows good short-term reproducibility.

"Federico II" University of Naples Hospital Management's Staff considered 47 informed consent forms in order to evaluate quality and quantity of the information transmitted to patients. Every form, distinguished by procedure (surgical, pharmacological, anesthesiologic or related to blood transfusions) was evaluated for the accuracy and validity of information related to: diagnosis, prognosis, diagnostic and therapeutic opportunities, expected benefits, adverse-side effects, iatrogenic risks, privacy policy on personal data. The forms were judged by information completeness criteria "conformed" or "not conformed" with standards. Our analysis demonstrate that physicians often are unaware of legal and ethical topics related to constructing informed consent forms. They usually omit crucial information or would use strict technical language. So far, we conclude Hospital Management's Staff definitively has a role in improving informed consent forms by establishing guidelines and promoting ethical issues. Final result could be to deserve stronger patient confidence in medical institutions.

The effects of the angiotensin converting enzyme (ACE) inhibitor captopril (SQ 14225) on intraocular pressure (IOP) were studied. Four groups were analyzed: group A, ten control subjects; group B, ten hypertensive patients with normal IOP; group C, ten normotensive patients with primary open angle glaucoma (POAG); and group D, ten hypertensive patients with POAG. Systolic and diastolic blood pressure, heart rate, pupil diameter, IOP and total outflow facility were recorded at baseline and at 1-h intervals up to 3h after an oral dose of 25 mg captopril or placebo, given in a randomized, double-blind cross-over fashion. The alternative treatment was given a week later. Captopril significantly lowered IOP in all patients, with no effects on heart rate and pupil diameter. Blood pressure changed only in patients with hypertension (groups B and D). Total outflow facility, measured by conventional tonography, increased significantly in all groups. These findings indicate that oral captopril could represent a new antiglaucomatous compound.

We evaluated the efficacy and safety of gallopamil 150 mg daily in middle-aged and elderly patients with stable exertional ischemia, using a medium-term randomized double-blind cross-over placebo-controlled trial. Twenty middle-aged patients (52.8 +/- 6 years; range 38-61 years) and 14 elderly patients (67.4 +/- 2.8 years; range 65-73 years) with stable exertional ischemia underwent a bicycle exercise test. After a run-in period, both groups received treatment with either placebo or gallopamil 50 mg tid for 28 days. At the end of this time, each patient crossed over to the alternate regimen. Gallopamil significantly reduced heart rate, blood pressure and rate pressure product (from 15.37 +/- 2.7 to 13.65 +/- 4.16 U x 10(-3); p < 0.01) in elderly patients at submaximal exercise, but had no effect in middle-aged patients (from 14.52 +/- 4.45 to 13.49 +/- 3.77 U x 10(-3); p = NS). At peak exercise, none of the hemodynamic parameters was modified with gallopamil in either group. At peak exercise, both middle-aged and elderly patients achieved rate-pressure products similar to those reached during placebo at higher work loads. Exercise duration and maximal work load significantly increased in both groups. Electrocardiographic signs of ischemia were favorably influenced by gallopamil in both groups (from 1.39 +/- 0.5 mm to 0.76 +/- 0.73 mm; p < 0.001 in the middle-aged patients and from 1.5 +/- 0.34 mm to 1 +/- 0.76 mm; p < 0.01 in the elderly patients).(ABSTRACT TRUNCATED AT 250 WORDS)

BACKGROUND We studied the effects of age and hypertension on responses to chronotropic dose (CD25) and standing-induced changes in the ratio of electrical systole (QT) to electromechanical systole (QS2) in order to identify their role on beta adrenoceptor sensitivity and to verify the value of QT/QS2 ratio as a noninvasive parameter of beta-adrenoceptor sensitivity. METHODS We enrolled 33 normal subjects and 37 hypertensive patients (WHO stage I and II) (age range 21-82 years). RESULTS CD25 was significantly age-related in normotensive and hypertensive subjects, whereas standing-induced QT/QS2 changes were age-related in normotensive subjects only When we divided subjects into three age groups, beta-adrenoceptor sensitivity was found to be lower in hypertensives than normotensives in the two groups under age 60, but was not affected in those over age 60. This suggests that hypertension influences beta-adrenoceptor sensitivity in younger subjects, but not in elderly patients, whose beta-adrenoceptor sensitivity is already reduced. CONCLUSIONS CD25 does not predict standing-induced QT/QS2 ratio changes; therefore, during autonomic stimulation, QT/QS2 ratio seems not to be significantly related to beta adrenergic sensitivity.