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Ochronosis is a disease of tyrosine metabolism. Although most commonly associated with alcaptonuria and spondyloarthropathy, cardiovascular abnormalities have been associated. We describe a case which exemplifies the cardiovascular findings in this entity.
An impedance plethysmograph recording was obtained on at least two occasions from 162 women between their 24 and 36th week of pregnancy; 29 while in labor and 21 at the time of their 6-week postpartum visit. There was a significant increase in venous capacitance and a decline in venous capacitance index during apparently normal pregnancy. Those with pregnancy complications (hypertension, premature labor and fetal growth retardation) appeared to have significantly abnormal venous reactivity. It is proposed that equal consideration be given to abnormal venous activity in the mechanisms and therapy of pregnancy-related cardiovascular abnormalities.
OBJECTIVE: To evaluate the interobserver agreement between physicians regarding a abnormal cardiovascular assessment on athletic preparticipation examinations. DESIGN: Cross-sectional clinical survey. SETTING: Outpatient Clinic, United States Military Academy, West Point, NY. PARTICIPANTS: We randomly selected 101 out of 539 cadet-athletes presenting for a preparticipation examination. Two primary care sports medicine fellows and a cardiologist examined the cadets. INTERVENTIONS: After obtaining informed consent from all participants, all 3 physicians separately evaluated all 101 cadets. The physicians recorded their clinical findings and whether they thought further cardiovascular evaluation (echocardiography) was indicated. MAIN OUTCOME MEASURES: Rate of referral for further cardiovascular evaluation, clinical agreement between sports medicine fellows, and clinical agreement between sports medicine fellows and the cardiologist. RESULTS: Each fellow referred 6 of the 101 evaluated cadets (5.9%). The cardiologist referred none. Although each fellow referred 6 cadets, only 1 cadet was referred by both. The kappa statistic for clinical agreement between fellows is 0.114 (95% CI, -0.182 to 0.411). There was no clinical agreement between the fellows and the cardiologist. CONCLUSIONS: This pilot study reveals a low level of agreement between physicians regarding which athletes with an abnormal examination deserved further testing. It challenges the standard of care and questions whether there is a need for improved technologies or improved training in cardiovascular clinical assessment.
Measurement of the time from onset to maximal or peak velocity (TPV) of pulmonary artery (PA) flow has been proposed as a noninvasive means of determining PA pressure. The effects of age, heart rate, increased PA pressure and flow, pulmonary valve obstruction and altered PA vascular resistance on this measurement were evaluated. In 84 children, aged 1 day to 18 years, TPV was measured using continuous-wave Doppler echocardiography. The children were separated into 3 groups. Group I (n = 33) consisted of children with no cardiovascular abnormalities. Group II (n = 33) consisted of children with a variety of cardiovascular diseases producing varying PA pressures and flows. Group III (n = 18) consisted of children who had valvular pulmonic stenosis with PA to right ventricular gradients greater than 40 mm Hg. Doppler studies of group II and III patients were performed in conjunction with measurement of PA pressures and flows at the time of cardiac catheterization. In group I TPV showed a significant negative linear correlation with heart rate (r = -0.86, p less than 0.001). The ratio of observed TPV to predicted TPV (TPVN) determined using the regression equation for TPV vs heart rate or TPV/TPVN was heart rate- and age-independent (p greater than 0.1) and ranged from 0.81 to 1.31 (mean 1.005). In group II TPV/TPVN was inversely related to the natural log of the PA pressures (systolic, r = -0.91; mean, r = -0.87; diastolic, r = -0.82; all p less than 0.01), whether pressure elevation was due to increased flow, resistance or left atrial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
White weanling rats were given intragastrically 4 doses of T-2 toxin (3 alpha-hydroxy-4 beta-1,5-diacetoxy-8 alpha-(3-methylbutyryloxy)-12,13-epoxytrichothec-9-ene) a secondary metabolite of certain Fusarium species, 6 out of 9 treated rats developed increased blood pressure; these animals showed microscopically severe cardiovascular abnormalities. Occasional contamination of foodstuffs wh Fusarium may contribute to hypertension and cardiovascular lesions in animals and man.
Cardiovascular abnormalities have been considered important extrarenal manifestations of autosomal dominant polycystic kidney disease (ADPKD). However, little is known about their prevalence in patients with ADPKD undergoing hemodialysis (HD). To investigate whether cardiac abnormalities are more prevalent in these patients, clinical and echocardiographic manifestations of cardiovascular disease were evaluated in a group of 32 patients with ADPKD and a matched control group of 32 patients without diabetes treated by chronic HD for more than 6 months. Predialysis systolic and diastolic blood pressure (BP), prevalence of hypertension, and number of patients requiring antihypertensive medications were lower in the ADPKD group than controls. There was no difference in the prevalence of cardiac events, including cardiac failure, ischemic heart disease, and arrhythmia. Systolic dysfunction, diastolic patterns, and left ventricular hypertrophy were similar in the two groups. In patients with ADPKD, simple regression analysis showed left ventricular mass (LVM) index was correlated with hemoglobin level and predialytic systolic and diastolic BPs. In multiple regression analysis, predialysis systolic BP was the only independent variable linked to LVM index. The prevalence of aortic, mitral, and tricuspid valve disease did not differ between groups. In conclusion, the occurrence of cardiovascular complications in patients with ADPKD is similar to that of HD patients with other primary renal diseases, although hypertension is less prevalent.
Sudden Unexplained Death Syndrome (SUDS) is a major health problem in rural residents of Northeast Thailand. The cause of death in SUDS is suspected to be cardiovascular abnormalities. As magnesium (Mg) and zinc (Zn) deficiency contribute significantly to several cardiovascular diseases, we investigated the Mg- and Zn-status of patients with sudden respiratory distress and cardiac arrest who had survived resuscitation attempts or a near-SUDS episode (N-SUDS). The following subjects were enrolled: 12 N-SUDS inhabitants of rural Northeast Thailand (rural group 1, R1), 13 rural villagers with no past history of N-SUDS (rural group 2, R2), 15 urban Northeasterners (urban group 1, U1); 13 Bangkokians (urban group 2, U2). All subjects were free of structural heart disease. Magnesium and zinc were assessed by atomic absorption spectrophotometry of samples of plasma, red blood cells (RBC), white blood cells (WBC), and 24-hour urine. The mean levels of magnesium in the RBC, WBC, and 24-hour urine of N-SUDS patients (R1) were significantly lower than those of the urban groups (U1 and U2), while the plasma levels did not show any differences. When comparing the Zn-status of R1 with that of the urban groups (U1 and U2), the plasma, RBC, and WBC levels were found to be significantly lower in R1 (except for the RBC-Zn of the U1 group), while the 24-hour urine levels was higher. Although the magnesium and zinc parameters were not significantly different between the rural groups R1 and R2, the prevalence of hypomagnesuria (<2.2 mmol/day), hypozincemia (<9.7 micromol/l), and hyperzincuria (>10.7 micromol/day) was higher in the R1 group. These findings suggest that the homeostasis of both magnesium and zinc is altered in N-SUDS patients. Similar alterations, to a lesser degree, were observed in those people living in the same rural environment (R2).
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Sudden cardiac death is a rare but devastating event. The majority of cases in young athletes are caused by congenital cardiac abnormalities that are routinely clinically silent before causing sudden death. An optimal screening practice to help identify underlying asymptomatic cardiac abnormalities has met with much debate. Beyond the American Heart Association's recommendations for cardiovascular screening guidelines for the preparticipation physical examination [47], there are conflicting views regarding the use of more advanced diagnostic screening tests. Athletes in whom a potentially life-threatening cardiovascular abnormality is found face the probability of being restricted from participating in certain types of athletic activity. Participation guidelines for athletes with cardiovascular disease are detailed in the recommendations of the 26th Bethesda Conference [36]. Future goals should continue to focus on the prevention of SCD. The development of a cost-effective screening process that incorporates the use of echocardiography, although having its own set of inherent limitations, may prove to be the most viable option.
Understanding normal and abnormal cardiovascular development is of interest to basic scientists as well as to clinicians taking care of infants with heart defects. This article presents a visual overview of cardiac development. It provides a framework on which to understand how abnormal cardiac development leads to groups of cardiovascular defects requiring clinical care. Human heart development is presented schematically and is correlated with similar points in chick cardiac development. Studying both normal and abnormal cardiac development in neural crest-ablated embryos has highlighted two major themes of cardiac development: there is a mechanism of differential growth in the developing cardiovascular system that is not seen to a major extent after birth and cardiac defects can be pictured as arrested stages of normal development. At a particular stage of development, it is normal to have a certain relationship between developing structures. However, if the development is arrested and this relationship of structures is allowed to persist, it then becomes abnormal. Visualizing heart defects as arrested points in normal development is better used as a tool to categorize defects than as a causative mechanism. The exact mechanisms of how abnormal development results in cardiac defects is not well understood. Study of the neural crest model of cardiac defects suggests possible mechanisms.
This study was undertaken to identify all congenital heart disease in infancy, including deaths before diagnosis, to provide a truer picture of the spectrum of congenital heart disease and to assess the 'treatability' of those dying before diagnosis. All births, infant deaths, and surviving babies with congenital heart disease in one health region in 1985-90 were identified and were classified as 'complex', 'significant', or 'minor'. Of the 1074 infants diagnosed in infancy, 185 died and 56 of these (30%) died undiagnosed. Severe non-cardiac malformations were present in 29 of the 56 while 27 were otherwise normal. Cardiovascular abnormalities in the latter group were complex in 13/27 and significant in 14/27. Identification of undiagnosed cardiovascular anomalies will improve epidemiological evaluation of congenital heart disease and, more importantly, earlier recognition of treatable abnormalities may reduce mortality.
Knowledge of early developmental circulatory physiology has lagged behind advances in molecular cardiology. Cardiovascular physiology changes during embryonic development in a highly complex and carefully orchestrated manner, tightly correlated with structural development. Circulatory changes in early development include increasing heart rate, preload, and cardiac output; decreasing peripheral resistance; and increasing ventricular compliance, paralleling the increasing metabolic needs of the growing embryo. Newer techniques and the recent ability to study mammalian models of development have led to further insight into changes in myocardial and peripheral vascular physiology. The next major challenges include understanding the mechanisms regulating cardiovascular hemodynamics, normal physiologic adaptation of the growing embryo, and the physiology of abnormal cardiovascular development.
The clinical implications of newly acquired left bundle-branch block (LBBB) were examined prospectively in the Framingham Study population. During 18 years of observation 55 people developed LBBB. The mean age at the onset of LBBB was 62; LBBB occurred largely in people with antecedent hypertension, cardiac enlargement, coronary heart disease, or a combination of these. Coincident with or subsequent to the onset of LBBB, 48% developed clinical coronary disease or congestive failure for the first time. Throughout the entire period of observation only 11% remained free of clinically apparent cardiovascular abnormalities. Within 10 years of the onset of LBBB, 50% had died from cardiovascular diseases. In men, the appearance of LBBB contributed independently to an increased risk of cardiovascular disease mortality. Comparison with age- and sex-matched control subjects free from LBBB confirmed that in the general adult population, newly acquired LBBB is most often a hallmark of advanced hypertensive or ischemic heart disease, or both.
Treatment of arterial hypertension is an important part of medical care provided in industrialized countries today. When non-drug treatment turns out to be ineffective, or when hypertension levels are higher than target values, or target organ damage is ascertained, drug therapy must be started. This rationale comes from large-scale intervention trials, which have shown that the lowering of elevated blood pressure reduces cardiovascular morbidity and mortality. A logical aim in treatment of hypertension should be both to "normalize" hypertension-induced cardiovascular abnormalities and to maintain the quality of life, without undesirable influence on other cardiovascular risks. Moreover, if we could identify the major hemodynamic impairment behind increased blood pressure and correct it by an appropriate drug therapy, then we would have a satisfactory means to perform individualized treatment. Over the past years the empirical basis for the use of antihypertensive drugs has been replaced by a step-wise approach, but few attempts have been made to provide an approach that fits pathophysiological understanding. For this reason the above-mentioned step-wise approach has been found to be an uncorrected simplification of antihypertensive care. Also, the use of more recent drugs (calcium channel blockers, ACE-inhibitors and serotonin-receptor blockers) as an alternative to beta-blockers and diuretics in first step therapy, has further contributed to the abandonment of the step-wise approach. The different groups of antihypertensive agents are examined with reference to their mechanism of action, pharmacokinetics, indications, and desirable and untoward effects. At present, indirect vasodilators, such as calcium-antagonists, ACE-inhibitors and serotonin-receptor blockers, alone or combined with diuretics, represent an intrinsic part of basic antihypertensive therapy. Beta-adrenoceptor antagonists remain the agents of choice when the principal therapeutic aim is to reduce the adrenergic drive. Both these drugs and direct vasodilators or alpha-adrenoceptor antagonists can be employed in the most severe forms of hypertension. In such cases, combined therapy (vasodilator + antiadrenergic + diuretic agents) is often used. Sublingual nifedipine and intravenous diazoxide or sodium nitroprusside are the drugs of choice for the hypertensive crisis. The use of most of the central or peripheral sympatholytic agents has generally been abandoned. Finally, beta-blockers and calcium-antagonists have been shown to have a secure place in the management of ischemic heart disease complicating arterial hypertension. In this condition captopril also appears to be useful.
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The sweatspot test assesses the local sweat response to an intradermal injection of acetylcholine. It has been reported as a more sensitive indicator of autonomic dysfunction in important diabetic men than either pupillary or cardiovascular tests, and has been used to establish the presence of autonomic dysfunction in patients with idiopathic chronic constipation. However, the usefulness of this test as a simple and quick method of diagnosing autonomic dysfunction in an elderly population has not been established. This is important given the high prevalence of reduced autonomic function with ageing and hypertension. We compared the age-associated responses in the sweatspot test and its relation to cardiovascular autonomic function in elderly normotensive and hypertensive subjects. We studied eleven normotensive and 24 untreated hypertensive elderly subjects (mean age 75.7 years, range 63-85) and compared the results of the sweatspot test to a young control group (n = 11, mean age 32.0 years, range 25-41), and to a standard battery of cardiovascular autonomic function tests. The median sweatspot score was significantly lower in the elderly compared with young subjects (1.9 vs. 12.0, p < 0.0001) although there was no difference between elderly normotensive and hypertensive subjects (1.6 vs. 2.4, p = 0.8). No correlation was demonstrated between the median sweatspot score and the number of abnormal cardiovascular tests. The sweatspot test was grossly abnormal in all elderly subjects and was not correlated to changes in cardiovascular autonomic function. Its diagnostic use in the elderly is therefore of very limited value.