Risk factors and clinical features of leukoaraiosis.
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Publications and source records attributed to C Marini.
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Essential hypertensives are at greater risk for ventricular arrhythmias than normotensive controls. A reduction in coronary flow reserve may be one of the mechanisms underlying this increased prevalence of ventricular dysrhythmias in hypertensives. It has previously been shown that dipyridamole infusion may provoke ischemic-like S-T segment depression in essential hypertensives with angiographically normal coronary arteries and reduced flow reserve. The aim of the present study was to assess whether electrocardiographic positivity (S-T segment depression greater than 0.1 mV from baseline) during dipyridamole testing (12-lead electrocardiogram and two-dimensional echomonitoring, with the infusion of 0.84 mg/kg dipyridamole over 10 min) might identify hypertensives at greater risk for ventricular dysrhythmias. We therefore studied 51 mild-to-moderate essential hypertensives by dipyridamole testing and 48-h Holter monitoring. All patients were off therapy for at least 2 weeks before testing and Holter evaluation. Left ventricular mass (by Penn convention) and ejection fraction (by Teichholtz rule) were evaluated by two-dimensional echocardiography. Lown classes 0-1 were found in 31 patients (Group 1) and Lown classes II-IV in 20 (Group 2). The two groups overlapped for mean blood pressure (121 +/- 9 versus 124 +/- 8 mmHg), left ventricular mass index (120 +/- 27 versus 141 +/- 42 g/m2) and left ventricular ejection fraction (54 +/- 6 versus 52 +/- 6). An electrocardiographically-positive dipyridamole test was found in seven of Group I and 16 of Group II patients (23 versus 80%, P less than 0.01). No patient showed a transient, either regional or global, systolic dysfunction during dipyridamole testing.(ABSTRACT TRUNCATED AT 250 WORDS)
Two-dimensional echocardiography is the best means of identifying early cardiac amyloid infiltration and gauging its subsequent progression. The early asymptomatic phase is characterized on echocardiography by a mild-to-moderate increase in left ventricular and/or right ventricular wall thicknesses. The distinctive combination of low electrocardiography voltage and increase in left ventricular mass on the echocardiogram, both compatible with substantial amyloid infiltration, is valuable in diagnosis and appears to indicate the severity of the disease. Other ancillary but common findings are left atrial dilatation, a small pericardial effusion, thickening of cardiac valves, papillary muscles, and interatrial septum. Finally, there is a peculiar texture of myocardial walls, with highly refractile areas that are typical, although not specific, of myocardial amyloidosis and can also be quantitatively described by digital image analysis techniques. The echocardiographic appearance of amyloidosis can closely mimic several other diseases. Asymmetric hypertrophy of the septum due to amyloid deposition may occur, simulating hypertrophic cardiomyopathy. The granular sparkling of myocardial walls is also found in myocarditis with severe fibrosis, and it is quite common in hypertrophic cardiomyopathy, as well as in other infiltrative diseases of the myocardium. It is not uncommon that the echocardiographic examination represents a turning point in the work-up of the patient, briskly orienting the clinician towards the correct diagnostic pathway. However, the likelihood of the cardiologist-echocardiographer to successfully and prospectively identify myocardial amyloidosis is substantially higher if all the clinical and electrocardiographic information is reviewed at the time of the echocardiographic examination.
A morphological restructuring of cardiac and arteriolar tissue is common in hypertension. The parallel evolution of these two processes as a compensatory response to pressure overload is a frequently assumed but unsubstantiated hypothesis. To evaluate this possibility, we have concomitantly measured left ventricular mass (LVM; two-dimensional echo) and minimal forearm vascular resistance (FVR; derived from the ratio of intra-arterial blood pressure: forearm blood flow by venous plethysmography) at maximal postischemic (13 min ischemia + 1 min hand exercise) reactive hyperemia. The study was performed on 29 essential hypertensive patients (15 males, 14 females, aged 50 +/- 10 years) who had not been undergoing treatment for hypertension for at least 15 days at the time of study. Minimum FVR was taken as a hemodynamic index of the integrated arteriolar lumen at the forearm level. LVM index and minimum FVR ranged from normal to clearly altered values. In spite of a wide spread of values, no correlation existed between the individual values of the two variables. Systemic mean blood pressure correlated with minimum FVR and tended to correlate with LVMI. Thus, morphological restructing of cardiac and arteriolar tissue does not seem to evolve in parallel in human hypertension. Pressure overload may contribute to cardiovascular hypertrophy, but other unrelated mechanisms may also underlie the development of cardiac and arteriolar abnormalities of human hypertension.
Arterial hypertension can provoke a reduction in coronary flow reserve through several mechanisms that are not mutually exclusive, namely, coronary artery disease, left ventricular hypertrophy, and microvascular disease. These different targets of arterial hypertension should be explored with different diagnostic markers. The transient dyssynergy detected by two-dimensional echocardiography and evoked during dipyridamole infusion is a marker of coronary disease that is equally reliable in normotensive and hypertensive individuals. On the contrary, dipyridamole-induced ST segment depression is frequently elicited in hypertensive patients when angiographically assessed coronary disease is absent. This ischemiclike electrocardiographic response can be found in echocardiographically assessed left ventricular hypertrophy. However, even when left ventricular mass is normal, dipyridamole-induced ST segment depression is associated with an impaired coronary flow response to pacing, which is consistent with microvascular disease. Whether echocardiographically silent electrocardiographic changes are simply diagnostic noises transmitting a misleading false positive response or a potentially important clinical marker of early myocardial damage remains a pivotal though still unanswered question.
Atrial natriuretic factor (ANF) release is modulated by several haemodynamic factors, including ventricular and atrial wall stretch. Dipyridamole infusion, which is commonly used as a pharmacological stressor in patients with coronary artery disease, can acutely increase ventricular and atrial pressure via myocardial ischaemia. The aim of this study was to assess whether dipyridamole infusion (up to 0.84 mg kg-1 over 10') can affect ANF release in man. Nineteen patients (13 men, 6 women) with a history of chest pain were studied. Their drug regimen was interrupted and instead they were administered a dipyridamole infusion, combined with two-dimensional echocardiography and 12-lead ECG monitoring. Plasma ANF was measured by RIA while the patients rested, and after dipyridamole infusion. Eight patients had no evidence of myocardial ischaemia, as measured by electrocardiographic and/or echocardiographic criteria, during dipyridamole infusion: among them, ANF values were similar while they were at rest and at peak dipyridamole administration (23.9 +/- 9.5 vs 23.4 +/- 6.9 pg ml-1, P = ns). Eleven patients had dipyridamole-induced transient ischaemia (regional ventricular dyssynergy and/or ST segment depression): among them, ANF values rose significantly at peak dipyridamole administration (31.8 +/- 13.8 vs 65.5 +/- 36.4, P less than 0.01). We conclude that dipyridamole infusion does not increase ANF release in man in the absence of ischaemia. The induction of myocardial ischaemia acutely increases ANF release, probably through a rise in ventricular and atrial wall stress.
In order to study the role of genetic factors in multiple sclerosis, cytogenetic analysis was performed on 48 patients with the clinically defined disease. We found a high incidence of subjects (50%) with abnormal chromosomes, showing premature centromere division of the X chromosome and structural aberrations, translocations, or deletions that could suggest preferential breakpoints. Correlation between clinical and cytogenetic data showed that cytogenetic abnormalities were more common in patients with high frequency of relapse or with a progressive form of the disease.
The success rate of laser-assisted microvascular anastomosis (LAMA) can be influenced by many factors, including the parameters of the laser technique used. This study examined the effects of laser pulse duration and the occurrence of anastomotic disruption immediately following first repair attempts on the incidence of aneurysm formation and the patency rate in LAMA. Fifty transected rat femoral arteries in 25 rats were anastomosed with three stay sutures and welded with a CO2 laser at a power of 80 mW. In each rat, the laser was applied in the form of 45 pulses of 0.2 sec duration to one femoral artery (group 1) and in the form of 15 pulses of 0.6 sec duration to the contralateral femoral artery (group 2). Comparison of group 1 with group 2 showed that overall rates of aneurysm formation (30% vs. 17%) and patency rates (92% vs. 96%) did not differ significantly (P less than 0.05) at 3 weeks postoperatively. However, disrupted vessels in both groups had a significantly higher incidence of subsequent aneurysm formation than nondisrupted vessels (54% vs. 0% in group 1, P less than 0.05; 43% vs. 6% in group 2, P less than 0.06; groups 1 and 2 pooled, P less than 0.001). These findings indicate that changes in laser pulse duration such as those tested do not affect the aneurysm and patency rates of LAMA. The results demonstrate, however, that disruption after laser welding plays a significant role in subsequent aneurysm formation.
7 patients with relapsing-remitting multiple sclerosis (MS) were subjected to an intensive course of intravenous (I.V.) cyclophosphamide (CY) therapy. All patients received induction therapy with 11 daily doses of 300 mg/m2 and then a single dose every six months for three years. After one year of follow-up all patients showed a decrease in relapse rate (0.57.57); in the two subsequent years of follow-up 2 patients showed a mild worsening while the others were clinically stable. As suggested by others, our results indicate that I.V. CY therapy may influence the clinical course of relapsing-remitting MS.
Included in this study are all patients with trauma to the parotid region seen at our center from 1979 to 1989. There was a total of five patients with injury to the parotid area: two patients with isolated facial nerve injury; one with isolated parotid duct injury; two with combined duct and nerve injury. There were four males and one female, with a mean age of 34 years (range, 16 to 62 years). The three patients with parotid duct injury required other procedures for associated trauma. A total of eight nerve branches were severed in four patients. Seven of the eight nerve branches (82.5%) were primarily repaired, with excellent functional results. Two of the three ductal injuries were repaired primarily over a stent, and one was ligated. No complications resulted from either treatment. Based on our clinical experience and review of the literature, we suggest that the treatment of parotid region injuries should include: 1) a complete initial assessment; 2) primary repair of parotid duct transection within 24 hours when possible; 3) primary repair of all facial nerve injuries, although delayed nerve repair remains a viable alternative; and 4) nonsurgical treatment of sialoceles and fistulae.
We subjected anesthetized mechanically ventilated rabbits (n = 6) to sequential exchanges of blood for a 6% dextran solution and compared their responses with those obtained in a previous study on progressive hypoxemia (n = 7). Right atrial PO2 (PVO2)RA and hindlimb PO2 (PVO2)limb, measured at the level of the iliac bifurcation, were compared with tissue PO2 (PtiO2) histograms obtained with an array of surface microelectrodes placed over the biceps femoris muscle. Systemic O2 consumption (VO2) was measured with the expired gas method. Cardiac output and systemic O2 transport (TO2) were calculated. Six exchanges of blood for dextran produced decreases in hemoglobin from 10.8 +/- 0.4 to 2.7 +/- 0.2 g/dl (P less than 0.001). Critical TO2 (TO2crit), defined as the level of TO2 associated with initial decreases in control VO2, was similar for anemia and hypoxemia (40.5 +/- 5.6 and 40.1 +/- 5.3 ml.min-1.kg-1, respectively). At any given TO2 other than control TO2, the levels of (PVO2)RA and (PVO2)limb were greater in anemia than in hypoxemia (P less than 0.01), but the mean and the distribution of the PtiO2 histograms were similar in both conditions. Mean PtiO2 was significantly less than (PVO2)RA or (PVO2)limb, except for those values obtained during the control period. These results confirm our previous finding that PVO2 is not an accurate index of PtiO2 under conditions of tissue hypoxia. Furthermore, similar PtiO2 levels during anemia and hypoxemia suggest that VO2 is limited by decreases in O2 diffusion from the capillaries to the cells.
In asymptomatic patients with essential hypertension, electrocardiographic changes suggestive of myocardial ischemia can be elicited by rapid pressure lowering or by pronounced coronary arteriolar dilation. The aim of this study was to assess whether dipyridamole infusion might induce ischemic-like electrocardiographic changes in asymptomatic essential hypertensive patients and to describe the clinical and echocardiographic correlates possibly associated with this response. We therefore studied a control group of 20 normotensive individuals and a group of 28 asymptomatic patients with mild-to-moderate essential hypertension. All underwent dipyridamole-echocardiography testing (12-lead electrocardiogram and two-dimensional echocardiographic monitoring with dipyridamole infusion, 0.84 mg/kg over 10'). No patient showed transient regional dyssynergy during dipyridamole infusion. None of the normotensive and 10 of 28 of the hypertensive participants had horizontal or downsloping ST segment depression more than 0.1 mV during dipyridamole (0% versus 36%, p less than 0.01). Hypertensive patients with ("responders") (n = 10) and without ("nonresponders") (n = 18) ST segment depression showed similar values of percent fractional shortening in baseline conditions (32 +/- 5 versus 33 +/- 6, p = NS) and at peak dipyridamole infusion (45 +/- 8 versus 43 +/- 5, p = NS). The peak early to peak late velocity ratio values (evaluated from transmitral flow tracings by Doppler technique) were also similar in baseline conditions (0.86 +/- 0.14 versus 0.94 +/- 0.30, p = NS) and at peak dipyridamole (0.72 +/- 0.15 versus 0.78 +/- 0.32, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
The clinical features of 76 patients 5 to 14 years old suffering from primary headaches has been compared with those of 495 adults in the same diagnostic group. An association between migraine without aura and female sex was evident in both age groups, while an inversion of the usual M/F ratio was found in the younger group with other types of headache. Childhood headache attacks resulted to be less frequent, less severe and with a shorter duration than in adult patients. Also accompanying symptoms were less common in children than in adults. Furthermore pain was more often unilateral but less frequently pulsating in the younger group. These results point out the need for a different approach to childhood headaches.
The authors evaluated the efficacy and tolerability of treatment with ferritin in 40 cases of iron deficiency because of gynecological pathology. After 2 months of therapy, 80% of patients showed a normalization of laboratory examinations while after 4 months both the normalization of laboratory examinations and the clinical symptomatology, were demonstrated in all cases. Only 7.5% of cases were very light and did not show remarkable adverse. It is concluded that this can be used safely.
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Anesthetized mechanically ventilated rabbits were subjected to progressive hypoxemia (n = 7) to determine the relationship of venous PO2 (PvO2) to skeletal muscle PO2 (PtiO2). Measures of arterial PO2 (PaO2), right atrial PO2 [(PvO2)RA], and hindlimb PO2 [(PvO2)limb], were obtained from the carotid artery, right atrium, and inferior vena cava, just above the level of the iliac bifurcation. Biceps femoris muscle PtiO2 was measured with a surface O2 microelectrode having eight measuring points. PaO2 was decreased from 90.3 +/- 5.4 to 26.8 +/- 0.8 Torr in five consecutive steps, followed by reoxygenation to 105.6 +/- 10.5 (SE) Torr. Measurements were obtained after each decrement in PaO2. A total of 128 measures of PtiO2 were obtained per experimental stage. The mean and distribution of the muscle PtiO2 histogram were determined. Measurements were compared with analysis of variance and the Newman-Keuls post hoc method. (PvO2)limb had similar values as the average muscle PtiO2 (PtiO2) for PaO2 values greater than 52.1 +/- 4.3 Torr, where (PvO2)limb became greater than PtiO2 (P less than 0.05). The lowest measures of (PvO2)limb and PtiO2 were 15.9 +/- 0.7 and 4.0 +/- 0.1 Torr, respectively (P less than 0.01). The PtiO2 histograms showed no evidence of increased microvascular heterogeneity with hypoxemia. We conclude that in hypoxemia PvO2 is greater than muscle PtiO2. This difference may be related to the establishment of significant physicochemical O2 gradients from erythrocyte to tissue cell.
Leuko-araiosis (LA) is a descriptive term coined by Hachinsky et al. to indicate bilateral and nearly symmetrical areas of decreased density of the periventricular white matter and centra semiovalia seen on CT or MRI scan. These findings are frequently observed in elderly people, but they seem to be more frequent or more severe in demented patients regardless of the etiology. Neurological abnormalities observed in patients with LA are nonspecific and insufficient to describe a definite clinical picture. The hypothesis that LA could be vascular in origin, even in Alzheimer patients is attractive but unproven.
The incidence of chronic pancreatitis has been increasing in the western world. Although chronic alcohol abuse accounts for 90% of adult cases, the physician must be aware of the multiplicity of causes for chronic pancreatitis. We present a case of obstruction of the pancreatic duct and chronic pancreatitis caused by a primary carcinoid tumor.