Lessons learnt from a pilot study on residual dye removal by an aerated treatment wetland.

Treatment wetlands (TWs) have shown good capacity in dye removal from textile wastewater. However, the high hydraulic retention times (HRTs) required by these solutions and the connected high area requirements, remain a big drawback towards the application of TWs for dye treatment at full scale. Aerated TWs are interesting intensified solutions that attempt to reduce the TW required area. Therefore, an aerated CW pilot plant, composed of a 20 m2 horizontal subsurface flow TW (HF) and a 21 m2 Free Water System (FWS), equipped with aeration pipelines, was built and monitored to investigate the potential reduction of required area for dye removal from the effluent wastewater of a centralized wastewater treatment plant (WWTP). During a 8 months long study, experimenting with different hydraulic retention times (HRTs - 1.2, 2.6 and 3.5 days) and aeration modes (intermittent and continuous), the pilot plant has shown a normal biological degradation for organic matter and nutrients, while the residual dye removal has been very low, as demonstrated by the absorbance measure at three wavelengths: at 426 nm (blue) the removal varies from -55% at influent absorbance of 0.010 to 41% at 0.060; at 558 nm (yellow) the removal is negative at 0.005 (-58%) and high at higher influent concentrations (72% at 0.035 of absorbance for the inlet); at 660 nm (red) -82% of removal efficiency was obtained at influent absorbance of 0.002 and 74% at 0.010. These results are a consequence of the biological oxidation processes taking place in the WWTP, so that the residual dye seems to be resistant to further aerobic degradation. Therefore, TWs enhanced by aeration can provide only a buffer effect on peak dye concentrations.

Relation between early mitral regurgitation and left ventricular thrombus formation after acute myocardial infarction: results of the GISSI-3 echo substudy.

OBJECTIVE: To evaluate the prevalence and correlates of left ventricular thrombosis in patients with acute myocardial infarction, and whether the occurrence of early mitral regurgitation has a protective effect against the formation of left ventricular thrombus. DESIGN AND SETTING: Multicentre clinical trial carried out in 47 Italian coronary care units. PATIENTS AND METHODS: 757 patients from the GISSI-3 echo substudy population with their first acute myocardial infarct were studied by echocardiography at 24-48 hours from symptom onset (S1), at discharge (S2), at six weeks (S3), and at six months (S4). The diagnosis of left ventricular thrombosis was based on the detection of an echo dense mass with defined margins visible throughout the cardiac cycle in at least two orthogonal views. RESULTS: In 64 patients (8%), left ventricular thrombosis was detected in one or more examinations. Compared with the remaining 693 patients, subjects with left ventricular thrombosis were older (mean (SD) age: 64.6 (13.0) v 59.8 (11.7) years, p < 0.005), and had larger infarcts (extent of wall motion asynergy: 40.9 (11.5)% v 24.9 (14)%, p < 0.001), greater depression of left ventricular ejection fraction at S1 (43.3 (6.9)% v 48.1 (6.8)%, p < 0.001), and greater left ventricular volumes at S1 (end diastolic volume: 87 (22) v 78 (18) ml/m(2), p < 0.001; end systolic volume: 50 (17) v 41 (14) ml/m(2), p < 0.001). The prevalence of moderate to severe mitral regurgitation on colour Doppler at S1 was greater in patients who had left ventricular thrombosis at any time (10.2% v 4.2%, p < 0.05). On stepwise multiple logistic regression analysis the only independent variables related to the presence of left ventricular thrombosis were the extent of wall motion asynergy and anterior site of infarction. CONCLUSIONS: Left ventricular thrombosis is not reduced, and may even be increased, by early moderate to severe mitral regurgitation after acute myocardial infarction. The only independent determinant of left ventricular thrombosis is the extent of the akinetic-dyskinetic area detected on echocardiography between 24-48 hours from symptom onset.

[Is a more efficient operative strategy feasible for the emergency management of the patient with acute chest pain?]. / E realizzabile una strategia operativa più efficace per la gestione in urgenza del paziente con dolore toracico acuto?

Patients with acute chest pain are a common problem and a difficult challenge for clinicians. In the United States more than 5 million patients are examined in the emergency department on a yearly basis, at a cost of 6 billion dollars. In the CHEPER registry the prevalence of patients with chest pain in the Emergency Department was 5.3%. Similarly, in 1997 at our institution the prevalence was 4.8%. Only 50% of the patients are subsequently found to have cardiac ischemia as the cause of their symptoms and 50-60% of them showed a non-diagnostic electrocardiogram (ECG). Twenty-five-50% of chest pain patients are not appropriately admitted to the hospital and despite this conservative approach, acute myocardial infarction is misdiagnosed up to 8% of patients with acute chest pain who are released from the emergency department without further evaluation, accounting for approximately 20% of emergency department malpractice in the United States. Important diagnostic information is covered by the patient's medical history, physical examination, and ECG, but often this approach is inadequate for a definitive diagnosis. Creatine kinase (CK) and CK isoenzyme--cardiac muscle subunit (CK-MB)--are traditionally obtained in the emergency department in patients admitted for suspected acute coronary syndrome. Mass measurements of CK-MB have improved sensitivity and specificity, and to date this is the gold standard test for diagnosis of acute myocardial infarction. CK-MB, however, is not a perfect marker because it is not totally cardiac specific and does not identify patients with unstable angina and minimal myocardial damage. There are no controlled clinical impact trials showing that these tests are effective in deciding whether to discharge or to appropriately admit the patient with suspected acute coronary syndrome. Relevant investigative interest has recently been focused on new markers for myocardial injury, including myoglobin, cardiac troponins T and I. Myoglobin, a sensitive but not specific marker for cardiac damage, increases earlier than CK-MB and cardiac troponins. It should be used early after symptom onset and in conjunction with a more specific marker of myocardial damage. Cardiac troponins T and I are highly specific markers for cardiac damage, rise parallel to CK-MB and remain elevated longer, up to 5 to 9 days. They are useful for detection of less severe degrees of myocardial injury, which may occur in several patients with unstable angina who are at higher risk of cardiac events. Recent studies suggest that cardiac troponins have good diagnostic performance and prognostic value in the heterogeneous population of patients seen in the Emergency Department with acute chest pain. Despite these promising data, several analytical and interpretative problems in the routine use of cardiac troponins must be solved. Incremental value of echocardiography in acute chest pain patients is still uncertain. Echocardiography can be recommended as an adjunctive test if readily available during acute chest pain or prolonged pain, especially in patients without previous myocardial infarction. Rest myocardial radionuclide imaging has been studied in the emergency department setting and although the overall diagnostic performance and prognostic value of sestamibi has been found to be promising, it is not suitable, in our country, for extensive clinical use. ECG exercise stress test in the emergency department population has been shown to be safe and it has a good negative predictive value for cardiac events. It should be recommended that any institution identify specific and shared protocol and strategies for management of patients with chest pain. These should include basal clinical evaluation, serial ECG and the use of specific and sensitive myocardial markers. Adjunctive tests, such as echocardiography, nuclear studies and stress tests should be employed when indicated taking into account local facilities.

Pharmacokinetic and pharmacodynamic effects of high-dose continuous intravenous verapamil infusion: clinical experience in the intensive care unit.

OBJECTIVE: Our study aimed at evaluating the pharmacokinetic, cardiovascular, and metabolic effects of high-dose verapamil continuous intravenous infusion in cancer patients. DESIGN: Prospective clinical and pharmacokinetic study. SETTING: Intensive care unit of a Cancer Research Institute. PATIENTS: Nine patients (age range 31 to 57 yrs) with progressive cancer disease and without cardiovascular, renal, or hepatic dysfunctions. INTERVENTIONS: After a loading dose (0.15 mg/kg followed by 12 hrs of continuous intravenous infusion at 0.20 mg/kg/hr), the infusion rate of verapamil was increased every 24 hrs (0.25, 0.30, 0.35, and 0.40 mg/kg/hr). The highest rate was maintained for 48 hrs. Doxorubicin was given from the 60 th to the 108 th hr. Hydrochlorothiazide (25 mg/day) and potassium (36 mmol/day) were given orally. Altogether, 17 courses were completed. MEASUREMENTS AND MAIN RESULTS: Steady state concentration (C(SS) and systemic clearance of verapamil and nor-verapamil (active metabolite) for each infusion rate were calculated. Mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), PR, QT and QTc intervals, and left ventricular ejection fraction (LVEF) were measured, as well as daily body weight, blood glucose and potassium. C(SS) of verapamil and nor-verapamil increased more than proportionally to the infusion rate (p<.001). Systemic clearance of verapamil decreased over the range of the infusion rate (p<.005). MAP and HR decreased at the 12th hr (p<.001) and then plateaued. CVP increased (p<.01). The relationship between MAP, HR, CVP, and verapamil plasma concentrations was significant (r2 = .25, .14, and .35, respectively; p<.0001). LVEF did not change. Six patients (11 courses) developed junctional rhythm. Three patients (six courses) showed a PR interval increase (p<.05). Patients with junctional rhythm had higher Css of verapamil (p<.009). Overall, QT and QTc intervals increased (p<.01). A linear relationship was observed between verapamil plasma concentrations and QT intervals (r2 = .09, p<.01). Cardiovascular side effects did not determine treatment withdrawal in any patient. Body weight, blood glucose, and potassium did not show significant changes. CONCLUSIONS: Our data suggest a capacity-limited clearance of high-dose verapamil. In the absence of heart disease, following a step by step increase of the dosage, the high plasma verapamil concentrations (617 to 2970 ng/mL) produce frequent but well tolerated hemodynamic and electrocardiogram changes.

Clinical impact of local implementation of agreed guidelines for the management of patients with acute myocardial infarction.

OBJECTIVE: This study sought to assess the impact of local implementation of clinical practice guidelines on the pattern of care and outcome in patients admitted to the Coronary Care Unit (CCU) with acute myocardial infarction. BACKGROUND: Development of clinical practice guidelines is among the most popular of the methods intended to promote translation of results from clinical trials into routine care. However, very little is known about the actual impact on routine care of the clinical guidelines for managing patients with acute myocardial infarction. METHODS: We reviewed a prospectively collected cohort of consecutive patients discharged with a diagnosis of acute myocardial infarction from S. Maria degli Angeli, a large community-based hospital in northeast Italy. Eighty-six patients treated in 1996 (before guideline implementation) were compared with 70 patients treated in 1997 (after guideline implementation) with respect to patterns of use of guideline-directed pharmacotherapies for acute myocardial infarction, diagnostic testing, length of CCU stay and clinical outcome. RESULTS: The two groups were similar in male gender, age, infarct location and severity. Patients managed before guideline implementation were less likely to receive thrombolysis (36 vs 50%; p = 0.05), i.v. beta-blockers at admission (13 vs 31%; p = 0.002), oral beta-blockers at CCU discharge (45 vs 74%; p = 0.0003). When these were given, patients managed before guideline implementation received lower dosages of i.v. heparin, as manifested by a lower proportion of patients reaching adequate aPTT levels at 24 hours (14 vs 62%, p < 0.0001), and of oral beta-blockers (-50%, p < 0.0001), and higher dosage of aspirin (+100%, p < 0.0001). The time to mobilization (+1 day) and the length of CCU stay (+0.5 day) were longer in patients managed before guideline implementation (p < 0.0001). Incidence of major complications was similar between the two groups (19 vs 13%, respectively; p = ns). CONCLUSIONS: Patients with myocardial infarction managed after local implementation of clinical practice guidelines were more likely to receive evidence-based effective pharmacotherapies, and to have earlier mobilization and earlier discharge from CCU. This study strongly supports the role of local implementation of clinical practice guidelines to optimize management of patients with acute myocardial infarction.

Prolonged treatment (2 years) with different doses (3 versus 6 MU) of interferon alpha-2b for chronic hepatitis type C. Results of a multicenter randomized trial.

BACKGROUND/AIMS: To examine the effect of prolonged treatment with different doses of interferon alpha-2b on the relapse rate in patients with chronic hepatitis C. METHODS: One hundred and seventy-one patients with non-cirrhotic chronic hepatitis C were enrolled in an Italian multicenter trial. All patients were treated for 3 months with 3,000,000 Units (3 MU) of interferon alpha-2b given subcutaneously three times a week (t.i.w.). Patients with abnormal alanine aminotransferase (ALT) values were given 6 MU of interferon for an additional 3 months. If ALT remained persistently abnormal, therapy was then suspended. If ALT levels were normal, therapy was continued (6 MU t.i.w.) for an additional 18 months (total=2 years). Patients with normal ALT were randomly assigned to two groups, one receiving 3 MU and the other receiving 6 MU t.i.w. for an additional 21 months (total=2 years). Follow-up continued for 2 years after therapy withdrawal. RESULTS: Seven patients stopped treatment during the first 3 months. Of the remaining 164 patients, 76 (46%) showed abnormal ALT levels after 3 months of therapy: 11 of these (14%) normalized ALT values when given 6 MU and a sustained response was maintained in eight during the follow-up. Overall, 54 and 34 patients were allocated respectively to the groups receiving the 3 MU and 6 MU long-term treatment. At the end of therapy, 35/54 patients of the group 3 MU and 21/34 patients of the group 6 MU showed normal ALT levels (65% vs 62%, p=N.S.). After 2 years of follow-up, 24/35 (69%) patients of the group 3 MU and 16/21 (76%) of the group 6 MU were still in remission (p=N.S.). In an intention-to-treat analysis, 48/171 (28%) patients showed a long-term response (normal ALT values, HCV-RNA negative). About 65% of the sustained responders showed low baseline viremia compared with 33% of non-responders (p=0.005) while genotype 1b was more frequently found among non-responders than in long-term responders (84% vs 25%, p=0.0001). CONCLUSIONS: About 14% of patients who do not respond to a 3-month course of 3 MU of interferon normalize ALT levels when given 6 MU. In prolonged treatment, there is no significant difference between 3 and 6 MU in inducing a sustained response. Patients with low baseline viremia and genotype 2a respond significantly better to prolonged interferon therapy than highly viremic patients with genotype 1b.

Effect of strength training on blood pressure measured in various conditions in sedentary men.

To examine the effect of long term strength training on heart rate and blood pressure, measured in different conditions, and on their variability, thirty healthy, previously sedentary men were randomized into a training and a control group. The strength training program consisted of 48 training sessions on a multigym apparatus at a frequency of 3 sessions each week, involving leg press, bench press, leg curl, shoulder press, leg extension and sit ups. The control group was asked not to change their sedentary lifestyle. In the subjects of the training group the load could be increased significantly for all exercises (p < 0.01). Heart rate and blood pressure were measured at rest in the supine and sitting position, during 24 hours with a non-invasive ambulatory device and during an exercise test on a cycloergometer. Repeated measures analysis of variance did not show an effect of strength training on heart rate or on blood pressure. In addition, power spectral analysis of the RR interval (ECG) and of the beat-to-beat blood pressure in the supine subject revealed similar total, low frequency and high frequency power before and after training, indicating that the neural control of both heart rate and blood pressure was not affected by a 16-week program of strength training.

Power spectral analysis of RR interval and blood pressure short-term variability at rest and during dynamic exercise: comparison between cyclists and controls.

To determine the adaptations of the autonomic nervous system in the control of heart rate and blood pressure induced by endurance training, 10 competitive cyclists aged 27 +/- 7 years and 10 age-, weight- and height-matched sedentary controls were subjected to Power Spectral Analysis of the RR interval and of blood pressure at supine rest and during submaximal cycloergometric exercise test in the supine position at 20% and 40% of maximal workload. At rest, the high-frequency (HF) power of the RR interval was higher in cyclists (p < 0.05) compared to controls, whereas the power spectrum of both systolic and diastolic blood pressure did not differ between cyclists and controls. During exercise the variance, the low-frequency (LF) and the HF power of the RR interval decreased significantly (p < 0.005) and similarly in cyclists and controls. The LF/HF ratio of the RR interval increased (p < 0.001) and the alfa index of baroreflex sensitivity decreased (p < 0.05) without differences between cyclists and controls. The variance of both systolic and diastolic blood pressure increased (p < 0.001 and p < 0.005, respectively) as well as the HF power of systolic blood pressure (p < 0.001) similarly in cyclists and in controls. In conclusion, the data of the present study suggest that competitive cycling causes an enhanced vagal drive to the sinus node, whereas the neural control of blood pressure is not affected. During exercise a vagal withdrawal and a sympathetic activation in the neural control of heart rate, together with a reduction of baroreflex sensitivity are operative. These changes are similar in cyclists and controls.

Signs of functional efferent reinnervation of the heart in patients after cardiac transplantation.

Short-term heart rate and blood pressure variability were assessed in 62 patients, studied within 1 month, at 1, at 2 or at 3-5 years after cardiac transplantation and in 13 healthy control subjects. Means and total variances were calculated and the powers of the low frequency (LF, 0.07-0.14 EqHz) and of the high frequency (HF, 0.14-0.35 EqHz) components were derived from power spectral analysis. Mean heart period, its total variance and the powers of the LF and HF components were lower in the transplanted patients than in the controls (P < 0.001). The total variance and the LF and HF powers differed significantly among the groups of transplanted patients (P < 0.01) and intergroup comparison showed significantly higher values in patients 3-5 years after transplantation than in those studied within 1 month. The variance of systolic blood pressure and its power spectrum did not differ between patients and controls. The results suggest that partial functional reinnervation of the sinus node occurs after heart transplantation in man.

Respiratory-related blood pressure variability in patients after heart transplantation.

Our objective was to study whether the variations of blood pressure synchronous with respiration depend on the simultaneous changes of heart rate. Power spectral analysis of the heart period or R-R interval, blood pressure, and respiratory activity was performed by fast Fourier transform during 30 min of supine rest in 12 patients between 16 and 23 days after orthotopic heart transplantation and in 12 age- and sex-matched normal control subjects. The components of the variations of the R-R interval and blood pressure associated with respiration [high-frequency (HF) components] were derived from the power spectra. The HF component of the power spectrum of the R-R interval was almost absent in the transplanted patients compared with the control subjects (2.9 vs. 104 ms2; P < 0.001), whereas the HF component of the power spectrum of blood pressure was not significantly different between the two groups (1.72 vs. 1.65 mmHg2 for systolic and 0.35 vs. 0.60 mmHg2 for diastolic blood pressure). Respiratory variations of both systolic and diastolic blood pressure in humans can depend only slightly on the respiratory heart rate variations.

Red blood cell sodium heteroexchange in familial primary hypertrophic cardiomyopathy.

The hallmark of primary hypertrophic cardiomyopathy is an inappropriate myocardial hypertrophy, linked to myofibril disarray of the left ventricle. Its variable clinical expression may be due to genetic heterogeneity and variable penetrance. Since we have recently shown that abnormalities of cation transport in the erythrocytes are associated with cardiac hypertrophy in essential hypertensives and insulin-dependent diabetics, we have investigated the relationship between cardiac anatomy and function and red cell Li+/Na+ and Na+/H+ exchange in 33 relatives of a patient who died of cardiac failure and was found to have a primary hypertrophic cardiomyopathy at autopsy. According to echocardiographic examination, 11 members of the family also had a hypertrophic cardiomyopathy, with a family distribution compatible with autosomal dominant genetic transmission and variable penetrance. Red cell Li+/Na+ and Na+/H+ exchange were not significantly different in the affected members as compared to the unaffected, but in the former, after correction for potentially confounding variables, interventricular septum thickness was positively correlated to Na+/H+ exchange and diastolic function (Area E/Area A and Vmax E/Vmax A) negatively correlated to Li+/Na+ exchange. Since a generalized overactivity of the cell membrane Na+/H+ exchange, reflected by increased Na+/H+ and Li+/Na+ exchanges in the red cells, could favour cellular growth and diastolic dysfunction, our data suggest that abnormalities of cell membrane cation transport could play a role in the phenotypic expression of hypertrophic cardiomyopathy.

Left ventricular performance during prolonged exercise and early recovery in healthy subjects.

The effect of semi-supine long lasting exercise to exhaustion [61 (SD 10) min] on left ventricular systolic performance was studied by echocardiography in 16 young healthy volunteers. During the incremental phase of exercise, the ejection fraction increased from 65.2 (SD 4.1)% to 80.1 (SD 4.8)% (P < 0.0001), then it levelled off up to the end of exercise [81.7 (SD 4.4)%, P < 0.0001 vs rest]. During recovery, the ejection fraction rapidly and steadily decreased to a value similar to that at rest [66.1 (SD 5.0)%, n.s.). A similar pattern was shown by the systolic blood pressure/end-systolic volume coefficient, which rose from 3.2 (SD 0.8) mmHg.ml-1 to 7.5 (SD 2.7) mmHg.ml-1 (P < 0.0001) in the initial phase and subsequently did not change until the end of exercise [7.0 (SD 2.2) mmHg.ml-1, P < 0.0001 vs rest], to fall sharply after the cessation of exercise [2.9 (SD 1.1) mmHg.ml-1 at the 10th min, n.s. vs rest]. Exercise and recovery indices of left ventricular performance were not correlated with exercise duration, maximal heart rate and increase in free fatty acids. The present results indicated that, after the initial increase, left ventricular performance remained elevated during prolonged high intensity exercise and that conclusions on exercise cardiac performance drawn from postexercise data can be misleading.

Age and blood-pressure-related changes in left ventricular diastolic filling.

PURPOSE: To evaluate the influence of different clinical and echocardiographic parameters on left ventricular diastolic filling in 66 mild to moderate hypertensives and 49 normotensives. METHODS: All subjects underwent an echocardiographic study with a pulsed Doppler evaluation of left ventricular filling. The hypertensive subjects also underwent non-invasive 24-h blood pressure monitoring. RESULTS: The ratio of early to atrial peak diastolic filling velocity and the ratio of the corresponding areas under the curve (AUC) were significantly lower in the hypertensives compared with the normotensives (P less than 0.001). In the hypertensives, office blood pressure, average 24-h mean blood pressure, the left atrial dimension and the left ventricular mass index were each related both to age and to diastolic filling. The variable most closely related to diastolic filling independently of age and the R-R interval was 24-h blood pressure (ratio of early: atrial peak filling velocity versus 24-h blood pressure: r = -0.307, P less than 0.05; ratio of early: atrial AUC versus 24-h blood pressure: r = -0.261, P less than 0.05). When the normotensives and hypertensives were each grouped according to age less than or equal to or greater than 40 years, the normotensive-hypertensive mean difference was greater in the subjects aged greater than 40 years for both the early:atrial maximal velocity ratio and the early:atrial AUC ratio. CONCLUSIONS: Age is the strongest clinical correlate for left ventricular diastolic function indices, in both hypertensives and normotensives. In the present study, average 24-h blood pressure and, to a lesser extent, the heart rate were also associated with an impaired diastolic performance.

[Left ventricular filling studied by echo-Doppler in hypertensive and normotensive subjects]. / Studio del riempimento ventricolare sinistro mediante eco-Doppler negli ipertesi e nei normotesi.

Purpose of the study was to evaluate the influence of different clinical and echocardiographic parameters on left ventricular diastolic filling in a group of 66 mild to moderate hypertensive subjects (mean age = 45.9 +/- 13.9 yrs) and in 49 normotensive controls (mean age = 44.2 +/- 15.9 yrs). All subjects underwent an echocardiographic study with pulsed Doppler evaluation of left ventricular filling. In the hypertensives, a noninvasive 24-hour blood pressure monitoring was performed. The ratio of early to atrial peak diastolic filling velocity (VmaxE/VmaxA) and the ratio between the respective velocity flow integral (Earea/Aarea) were significantly lower in the hypertensives compared to the normotensives (p less than 0.001). As within the hypertensives, office systolic blood pressure, average 24-hour mean blood pressure (24MBP), left atrial dimensions, and left ventricular mass index (MAXIND) were related both to age and diastolic filling. To study the relation between these parameters and diastolic filling a partial correlation test was used. The only variable related to diastolic filling, independently of age, was 24MBP (VmaxE/VmaxA vs 24MBP: r = -0.307, p less than 0.05, Earea/Aarea vs 24MBP: r = -0.261, p less than 0.05). Linear multivariate analysis using the method of stepwise regression established that age, 24MBP and heart rate were responsible for 75% of the VmaxE/VmaxA variance in the hypertensive group. To evaluate if the difference between the indexes of diastolic filling in the normotensives and the hypertensives varied according to age, we divided each group into two classes of subjects older and younger than 40 yrs. Under the age of 40 only VmaxE/VmaxA was significantly different in the two groups (p less than 0.05), while in the subjects older than 40 yrs both VmaxE/VmaxA and Earea/Aarea differed to a great level of statistical significance (p less than 0.001). The results of the present study allow the following conclusions: 1) age has the greatest influence on diastolic filling in both hypertensive and normotensive individuals. Diastolic filling is impaired in mild to moderate hypertension, when systolic function is still normal; 2) the worsening of diastolic filling determined by hypertension is more evident in the subjects greater than 40 yrs; 3) the only clinical variable that influences diastolic filling, independently of age, is 24MBP, while office blood pressure, MAXIND and left ventricular ejection fraction do not seem to be related to this clinical entity.

[Familial hypertrophic myocardiopathy: complex ventricular arrhythmias in healthy family members]. / Miocardiopatia ipertrofica familiare: aritmie ventricolari complesse nei parenti sani.

The aim of the present study was to evaluate the electrocardiographic changes among the members of a family affected by hypertrophic cardiomyopathy. Seventeen unaffected members and 8 affected members were studied by 24-hour Holter monitoring. Twenty-five normal controls were also studied by 24-hour Holter monitoring. One out of 7 (12.5%) patients with hypertrophic cardiomyopathy, 8 out of 17 (47%) unaffected relatives and 20 out of 25 (80%) controls did not show ventricular arrhythmias. One out of 7 patients (12.5%), 4 out of 17 (23.5%) unaffected relatives and 3 out of 25 (12%) of the control group showed Lown classes I-II ventricular arrhythmias. Complex ventricular arrhythmias (III-V Lown classes) were detected in 5/7 (71.4%) of patients, in 5/17 (29.5%) of unaffected members and only in 2/25 (8%) of the normals. Among the unaffected members we compared the prevalence of complex ventricular arrhythmias between the offspring of patients with that of the unaffected first-grade relatives. Three out 7 (43%) of the offspring of the patients showed complex ventricular arrhythmias and none among the offspring of normal first-grade relatives showed such arrhythmias. Neither the patients nor their relatives in this study showed any significant ST segment changes during the 24-hour Holter monitoring. We suggest that in first-grade relatives of patients with familial hypertrophic cardiomyopathy, complex ventricular arrhythmias could be a marker of latent disease, without clinical and echocardiographic manifestations.

Blood pressure changes during heavy-resistance exercise.

To study the mechanisms of the blood pressure changes during weight-lifting, three hypertensive and five normotensive body-builders underwent continuous intra-arterial monitoring. In two subjects (one normotensive and one hypertensive), intrathoracic and intra-abdominal pressures were also measured. Extremely high blood pressure elevations of up to 345/245 mmHg were observed during the lifts. Squatting caused the highest pressure rises and single-arm curls the lowest. Both the intrathoracic and the intra-abdominal pressures increased greatly during each lift and closely paralleled the changes in intra-arterial pressure. A close correlation was found between the blood pressure increase during the exercise and during a hand-grip test (r = 0.95, P less than 0.001). These results suggest that a pronounced increase in intra-thoracic and intra-abdominal pressures is a major determinant of the blood pressure elevations occurring during weight-lifting. The pressor reflex which accompanies static contractions and the individual baseline blood pressure levels also seem to affect the height of the pressure peaks.