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Pulse Pressure, Prehypertension, and Mortality: The San Antonio Heart Study

Prehypertension increases mortality risk. Pulse pressure is also associated with increased mortality. Nevertheless, the impact of pulse pressure on the relationship between prehypertension and mortality is not known in individuals who are free of diabetes and cardiovascular disease. Cox regression analysis was used to examine mortality risk among 3,632 (97.0%) participants in the San Antonio Heart Study (age range, 25-64 years; mean follow-up, 15.2 years). Results were adjusted for age, sex, ethnicity, education, body mass index (BMI), smoking, and total cholesterol concentration. The Seventh Report of the Joint Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) categories were used for blood pressure staging: normal, <120/80 mm Hg; prehypertension, 120-139/80-89 mm Hg. Prehypertension prevalence was 31.6% at baseline. There were 218 deaths during the follow-up period. Prehypertension-predicted mortality (all-cause, hazard ratio (HR) 1.49 (1.12-1.99); cardiovascular, HR 1.79 (1.07-3.02)). Relative to normal blood pressure plus pulse pressure in the lower tertile, prehypertension plus pulse pressure in the upper tertile was associated with increased mortality (all-cause, HR 2.14 (1.38-3.32); cardiovascular, HR 2.47 (1.13-5.39)); however, prehypertension plus pulse pressure in the lower tertile was not significantly associated with mortality (all-cause, HR 1.19 (0.52-2.67); cardiovascular, HR 0.43 (0.05-3.40)). Prehypertension increases mortality risk (all-cause and cardiovascular) in individuals who are free of diabetes and cardiovascular disease. Nevertheless, this relationship is not evident in individuals with narrow pulse pressure. Therefore, pulse pressure may be a relevant measure of blood pressure for the definition of normal blood pressure.

Acute Valvular Regurgitation

Acute severe valvular regurgitation is a surgical emergency, but accurate and timely diagnosis can be difficult. Although cardiovascular collapse is a common presentation, examination findings to suggest acute regurgitation may be subtle, and the clinical presentation may be nonspecific. Consequently, the presentation of acute valvular regurgitation may be mistaken for other acute conditions, such as sepsis, pneumonia, or nonvalvular heart failure. Although acute regurgitation may affect any valve, acute regurgitation of the left-sided valves is more common and has greater clinical impact than acute regurgitation of right-sided valves. Data to guide appropriate management of patients with acute regurgitation are sparse; there are no randomized trials, and much of the literature describes either small series or the experiences of specific centers. Despite these limitations, the available data are sufficient to allow identification of general principles as well as development of applicable guidelines from both the American College of Cardiology/American Heart Association and European Society of Cardiology. The guidelines recommend valve surgery for symptomatic patients with aortic or mitral regurgitation, including those with acute regurgitation.1–3 The data and guidelines emphasize overarching clinical principles, including the need for a high clinical suspicion of acute regurgitation, timely use of echocardiography, and, in the majority of patients, rapid progression to surgery. Causes of acute regurgitation overlap with causes of chronic regurgitation and vary depending on the valve affected (Table 1). Endocarditis may affect either the aortic or mitral valve, whereas other causes are unique to the specific valve involved. The majority of causes of acute regurgitation present as an acute or subacute event. However, acute regurgitation can occur in patients with chronic regurgitation, when regurgitant severity is exacerbated by factors such as coronary ischemia, chordal rupture, or leaflet perforation from endocarditis. Acute regurgitation of either the aortic or mitral valve may result from procedural …

Characterizing Blood Pressure, Heart Rate, Physical Activity, Circadian Rhythm and their Response to NOS Inhibitor and Substrate in CHF Rats with Telemetry

The radio-telemetric technology makes it possible to continuously monitor arterial pressure, heart rate and physical activity as well as their circadian rhythms and their response to therapeutics in unrestrained animals for a longer period of time. This is essential for in vivo cardiovascular research. The primary purpose of the present study was to use telemetry to characterize those physiological parameters in a rat model of heart failure post myocardial infarction. Moreover, some of the neurohormonal alterations and the hemodynamic responses to L-arginine, the substrate for nitric oxide synthase (NOS), and L-NAME that inhibits NOS activity were also evaluated. Rats with moderate and large myocardial infarction are considered to have chronic heart failure (CHF), which displayed decreased systolic and consequently decreased mean blood pressure, blunted diurnal dips in systolic, diastolic and mean blood pressure, narrowed pulse pressure and relatively reduced strength of physical activity. These telemetric alterations were accompanied by increased left ventricular end diastolic pressure, right and left ventricular hypertrophy and elevated plasma norepinephrine and tumor necrosis factor. In CHF rats, L-arginine widened pulse pressure and L-NAME caused attenuated pressor response, suggesting the presence of the general NO deficiency in this model. Thus, telemetry provides some new and unique information about CHF in rats, which is important in exploring the underlying mechanism of heart failure, but cannot be obtained by the conventional approach.

Interrater reliability of hemodynamic profiling of patients with heart failure in the ED

Objective Hemodynamic profiling (HP) of patients with heart failure (HF) based on clinical assessment of central congestion and peripheral perfusion has been widely used by cardiologists to help guide therapy and determine prognosis but has never been tested or validated in the emergency department (ED). We hypothesized that the interrater reliability of HP in the ED would be good or greater than 0.6. Methods Study design. This was a prospective, observational study. Setting. It was conducted in an academic suburban ED with emergency medicine residency. Subjects. A convenience sample of patients presenting to the ED with suspected acute decompensated HF was enrolled. Measures. Demographic and clinical information was collected using standardized data collection forms. Two emergency medicine physicians (masked to each other) evaluated all patients and classified them into 1 of 4 hemodynamic categories based on the presence or absence of central congestion (wet or dry) and peripheral hypoperfusion (cold or warm): warm and dry, warm and wet, cold and dry, and cold and wet. B-type natriuretic peptide levels, objective test of cardiac function, and final cardiologist diagnoses were obtained. Data analysis. Interrater reliabilities for overall hemodynamic profile and individual elements of congestion and perfusion were calculated using κ coefficients. Results Sixty-eight patients were enrolled. Their mean age was 72 ± 14 years, 53% were female, and 78% were white. Of the patients, 79% had a final diagnosis of HF. Most patients (>60%) were considered wet and warm. Interrater agreement for HP was 64%, κ = 0.28 (95% confidence interval, 0.01-0.51). Interrater agreement was poor to fair for all elements of congestion and perfusion except peripheral edema ( κ = 0.67) and a narrow pulse pressure ( κ = 0.66). Conclusions Hemodynamic profiling of patients with HF by emergency physicians in the ED is not highly reliable. One in 5 patients thought to have HF in the ED did not have a final diagnosis of HF.

Pharmacologic support of infants and children in septic shock.

Septic shock (SS) is a frequent cause for admission to the pediatric intensive care unit, requiring prompt recognition and intervention to improve outcome. Our aim is to review the relevant literature related to the diagnosis and management of SS and present a sequential management for its treatment. Non-systematic review of medical literature using the MEDLINE database. Articles were selected according to their relevance to the objective and according to the authors' opinions. The outcome of sepsis and SS is dependent on the early recognition and implementation of time-sensitive goal-directed therapies. These include rapid aggressive fluid resuscitation followed by a well-designed pharmacotherapy. The goals of the resuscitation are the restoration of microcirculation and improved organ tissue perfusion. Clinical and laboratory markers are needed to assess the adequacy of the treatments. Altered pharmacokinetic and pharmacodynamic responses dictate that vasoactive agents should be adjusted to achieve the predetermined goals. In initial resuscitation with isotonic solutions (> 60 mL/kg), either crystalloid (normal saline) or colloid infusion could be used. Despite adequate fluid resuscitation, if: (a) wide pulse pressure, low blood pressure, or bounding pulses (high cardiac output, low systemic vascular resistance--SVR) are present, norepinephrine should be considered; (b) prolonged capillary refill, weak pulses, narrow pulse pressure, normotensive (low cardiac output, high SVR), dopamine, epinephrine or dobutamine should be considered. Adjunctive therapy with stress dose of corticosteroid is indicated in selected populations. Septic shock hemodynamics is a changing process that requires frequent assessment and therapeutic adjustments.

Suporte farmacológico a lactentes e crianças com choque séptico

OBJETIVOS: O choque séptico (CS) é uma causa freqüente de internação na unidade de tratamento intensivo pediátrica e requer reconhecimento e intervenção imediatos para que haja um desfecho favorável. Nosso objetivo é revisar a literatura relacionada ao diagnóstico e manejo do CS e apresentar um manejo seqüencial para seu tratamento. FONTES DOS DADOS: Revisão não-sistemática da literatura médica através de pesquisa na base de dados MEDLINE. Os artigos foram selecionados de acordo com sua relevância em termos do objetivo proposto e com base na opinião dos autores. SÍNTESE DOS DADOS: O desfecho da sepse e do CS depende do reconhecimento precoce e da implementação de tratamentos sensíveis ao tempo e guiados por objetivos. Esses tratamentos incluem reanimação agressiva com fluidos seguida de tratamento medicamentoso bem elaborado. Os objetivos da reanimação são a restauração da microcirculação e a melhora da perfusão tecidual. Os marcadores clínicos e laboratoriais são importantes para avaliar a adequação dos tratamentos. Respostas farmacocinéticas e farmacodinâmicas alteradas indicam que os agentes vasoativos devem ser ajustados a fim de atingirem o objetivo pré-estabelecido. Na reanimação inicial com soluções isotônicas (> 60 mL/kg), é possível usar infusão tanto de cristalóides (solução salina normal) como de colóides. Apesar da reanimação adequada com fluidos, se: (a) uma pressão de pulso com grande amplitude, pressão arterial baixa, ou pulso oscilante (débito cardíaco alto, baixa resistência vascular sistêmica - RVS) estiverem presentes, o uso de noradrenalina deve ser considerado; (b) reenchimento capilar prolongado, pulso fraco e filiforme, pressão arterial normal (baixo débito cardíaco, alta RVS), deve-se considerar o uso de dopamina, adrenalina ou dobutamina. O tratamento concomitante com dose de estresse de corticosteróides é indicado em populações selecionadas. CONCLUSÕES: A resposta hemodinâmica do CS é um processo variável que requer avaliação e ajustes terapêuticos freqüentes.

Association of ACE genotype and predominantly diastolic hypertension: a preliminary study

The insertion/deletion (I/D) angiotensin-converting enzyme (ACE) polymorphism has been established as a cardiovascular risk factor in some populations, but the association with essential hypertension is controversial. Predominantly diastolic hypertension (PDH), or narrow pulse pressure hypertension, has been shown to have increased peripheral resistance. Because a DD genotype has been associated with higher plasma ACE levels and angiotensin II activity, we genotyped PDH patients for ACE I/D polymorphism. Ninety-three patients with systolic blood pressure (BP)<140 mmHg systolic and diastolic BP>90 mmHg, or BP>140/90 mmHg with a pulse pressure<45 mmHg, were defined as PDH. The II, ID and DD genotype variants of ACE were characterised by the triple primer nested-PCR method. Results were compared to 75 normotensive control individuals. Statistical significance was assessed by the Chi square test. The genotype distribution among PDH patients was II=20 (21.5%), ID=34 (36.5%), DD=39 (42%), while the distribution among normotensive controls was II=16 (21.4%), ID=42 (56%), DD=17 (22.6%). The difference in genotype distribution between PDH patients and controls was significant (p<0.02). ACE allele frequencies in PDH patients and controls were D=0.60, I=0.40 and D=0.51, I=0.49, respectively, statistically non-significant (ns). These results suggest an association between ACE genotype DD and predominantly diastolic hypertension.

Comparison of 60-Day Mortality in Hospitalized Heart Failure Patients With Versus Without Hypothermia

The use of aggressive treatments and the modification of current treatment in patients with heart failure (HF) relies heavily on the assessment of disease severity using prognostic markers. However, many such markers are unavailable in routine clinical practice, and others have little prognostic value. This study tested the hypothesis that low body temperature could predict short-term survival after discharge in patients hospitalized for HF. Data from the Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Congestive Heart Failure (ACTIV in CHF) trial, which randomized 319 patients hospitalized for HF to receive placebo or tolvaptan, were retrospectively analyzed. Hypothermia was defined a priori as an oral body temperature <35.8 degrees C at randomization. Cox regression was used to analyze survival within a 60-day follow-up period. Hypothermia was observed in 32 patients (10%). Mortality rates at 60 days after discharge were 6.3% (20 of 319) overall, 9.4% (3 of 32) in hypothermic patients, and 5.9% (17 of 287) in nonhypothermic patients. Hypothermia was a strong multivariate predictor of mortality; hypothermic patients were 3.9 times more likely to die within 60 days than nonhypothermic patients (95% confidence interval 1.002 to 15.16, p = 0.0497) after adjustment for treatment group, age, and other confounders. Hypothermia was associated with such indicators of low cardiac output as an elevated blood urea nitrogen/creatinine ratio, narrow pulse pressure, and a reduced ejection fraction. In conclusion, hypothermia appears to be a strong predictor of mortality in patients with HF.

Pulse pressure predicts prognosis in heart failure independent of invasive hemomdynamic parameters

Background: Pulse pressure (PP) is positively correlated with mortality in patients with hypertension. The association between PP and prognosis in patients with HF has not been systematically investigated. Methods: Our study analyzed 1879 systolic HF patients (age 52±13, LVEF 22±7, 60% NYHA IV) referred to a single university center for HF management and heart transplant evaluation between 1983 and 2003. Blood pressure, along with invasive hemodynamic variables, were prospectively recorded after implementation of HF medical therapy. Patients were analyzed by quartiles of systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP). Results: Patients with narrower PP were younger, had significantly lower LVEF and cardiac index, and higher pulmonary artery and pulmonary capillary wedge pressure (PCW). Decreased PP quartile was associated with male gender, lower Na and total cholesterol levels, and lower body mass index. Patients in lower PP quartiles were less likely to have history of hypertension or diabetes, and less likely to be treated with ACEIs and statins. PP quartiles were similar in terms of CAD, beta-blocker therapy, and levels of TnI, BNP, and Cr. Higher quartiles of PP were associated with significantly improved 1-yr survival, similar to the trends seen with SBP and DBP (Figure). Receiver operator curve analysis showed PP provided a similar degree of prognostic information as cardiac index (0.54 vs. 0.57, respectively) After adjustment for sex, age, CAD, LVEF, PCW and cardiac index, relative risk of death at 1 year per each 10 mmHg increase in PP was 0.88 95% CI 0.80-0.98) (p<0.02). Conclusions: Narrowed pulse pressure is associated with worsened outcomes in heart failure. Pulse pressure represents a simple noninvasive predictor of heart failure prognosis, providing information independent of invasive hemodynamic parameters and other heart failure prognostic factors .

Thyroid hormone and blood pressure regulation.

Thyroid hormone has well-recognized effects on the cardiovascular system and blood pressure regulation. Blood pressure is altered across the entire spectrum of thyroid disease. The effects of hyperthyroidism include increased cardiac output, contractility, tachycardia, widened pulse pressure, decreased systemic vascular resistance, and increased basal metabolic rate. The manifestations of hypothyroidism are in marked contrast to those of hyperthyroidism and include decreased cardiac output, narrow pulse pressure, increased systemic vascular resistance, and decreased metabolic rate. Although thyroid hormone affects almost all tissues of the body and mediates changes in homeostasis, adaptations of the cardiovascular system can result in changes in blood pressure to accommodate the new demands on the system. In this paper, we review the direct and indirect thyroid hormone-mediated effects on blood pressure.

Use of the original, modified, or new intracerebral hemorrhage score to predict mortality and morbidity after intracerebral hemorrhage.

A simple clinical scale of intracerebral hemorrhage (ICH), comprising the Glasgow Coma Scale score, age, infratentorial origin, ICH volume, and intraventricular hemorrhage, was recently shown to predict 30-day mortality. We studied how well the original ICH Score would predict morbidity and mortality and determined whether modification would improve the predictions. Patients admitted to a regional hospital with acute ICH in 1999 were reviewed. Independent predictors of mortality or good outcome (modified Rankin score <or=2) at 30 days were identified by logistic regression to devise a new ICH Score for comparison with the original Score. A modified Score was created by substituting National Institutes of Health Stroke Scale (NIHSS) for the Glasgow Coma Scale. The mortality rate was 22%, and 35% had good outcome. Independent factors for mortality were high NIHSS score, intraventricular hemorrhage, subarachnoid extension, and narrow pulse pressure. Independent factors for good outcome were low NIHSS score and low admission temperature. For all ICH Scores, no patient had a maximum score of 6. Cutoff values of >or=3 and <3 provided the best Youden's index of diagnostic test in all ICH Scores for mortality and good outcome, respectively. The original and modified ICH Scores predict mortality equally well. The new and modified ICH Scores are slightly better for prediction of good outcome. All 3 ICH Scores are simple clinical grading scales. As reliable predictors of good outcome and/or mortality, they are useful in clinical research studies and standardization of clinical protocols.

Cardiac tamponade caused by serous pericardial effusion in patients on extracorporeal membrane oxygenation

Purpose: Extracorporeal membrane oxygenation (ECMO) has been successful in the treatment of critically ill children; however, its use has been accompanied by a broad range of complications. The authors describe the presentation, clinical course, treatment, and outcome of 4 patients on ECMO in whom pericardial tamponade developed caused by a serous effusion. Methods: A retrospective review of patients placed on ECMO at our institution from 1993 to 1997 was performed. The case histories of 4 patients in whom pericardial tamponade developed caused by a serous effusion were reviewed in detail. Results: The first patient presented with hypotension while on venovenous (VV) ECMO. The hypotension improved with fluid resuscitation. The patient was converted from (VV) to venoarterial (VA) ECMO when hypotension recurred. After a third episode of hypotension, a narrow pulse pressure was noted, and echocardiography results confirmed a pericardial effusion. The diagnosis was recognized earlier in the course of the subsequent 3 patients. All 4 patients were treated with aspiration of serous fluid from the pericardium with an over-the-needle plastic catheter that was left in place. More than 1 aspiration was required in all cases. All 4 patients survived. Conclusions: The authors have identified a group of ECMO patients with pericardial tamponade caused by serous effusion with good response to treatment. A high index of suspicion and early echocardiography is warranted to confirm the diagnosis in a patient with hypotension on ECMO.

Isolated elevation of diastolic blood pressure. Real or artifactual?

Not infrequently, blood pressure measurement by the standard auscultatory technique yields a normal systolic pressure with an elevated diastolic pressure. The relatively narrow pulse pressure of such a measurement raises concern about the accuracy of the blood pressure measurement. The purpose of this study was to assess the accuracy of auscultatory blood pressure measurements in patients with an uncommonly narrow pulse pressure, particularly patients with an elevated diastolic but normal systolic pressure. Auscultatory blood pressure measurements were compared with an objective noninvasive standard, called K2 analysis, which has been shown to be more accurate than the auscultatory technique. Blood pressure was measured simultaneously by auscultatory and K2 techniques in 175 subjects. Comparisons were performed (1) in the group as a whole, (2) in four clinical subgroups (normotensive [< 140/< 90 mm Hg, n = 69], hypertensive [> or = 140/> or = 90 mm Hg, n = 53], isolated systolic hypertensive [> or = 140/< 90 mm Hg, n = 38], and isolated diastolic hypertensive [< 140/> or = 90 mm Hg, n = 15]), and (3) in two subgroups whose ratio of pulse pressure to diastolic pressure was greater than or equal to 0.45 (n = 151) or less than 0.45 (n = 24). Subjects in the isolated diastolic hypertensive group and in the group with a pulse pressure ratio less than 0.45 were considered to have a narrow pulse pressure. In the group as a whole, consistent with previous auscultatory-K2 comparisons, systolic pressure was slightly higher and diastolic pressure slightly lower when measured by K2 versus the auscultatory technique (auscultatory, 145/85 mm Hg; K2, 147/83 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Heart rate variability to monitor autonomic nervous system activity during orthostatic stress.

Exposure to microgravity with space flight, or to earth-based analogs such as head-down tilt (HDT) bedrest, results in cardiovascular deconditioning. With reapplication of gravity, deconditioning is most often observed as an elevated heart rate, a narrowed pulse pressure, and possibly even a failure to maintain blood pressure with symptoms of presyncope or syncope. Noninvasive measurements of heart rate variability (HRV) have been used to study cardiovascular control mechanisms during orthostatic stress (head-up tilt and lower body negative pressure [LBNP]). Recently, the authors developed a new approach to study heart rate and blood pressure control mechanisms. Coarse graining spectral analysis (CGSA) allows simultaneous extraction of not only parasympathetic (PNS) and sympathetic (SNS) indicators from the HRV signal, but also determines the fractal dimension (DF), calculated from the slope (beta) of the log spectral power-log frequency relationship. The fractal dimension is an index of the complexity of the cardiovascular control system. Our investigations have indicated patterns of HRV consistent with reduced PNS and increased SNS activity and reduced DF with the HRV signal during orthostatic stress. These findings also indicate that the cardiovascular system may be less stable when operating at a reduced level of complexity.

Electromechanical dissociation in newborns treated with extracorporeal membrane oxygenation

To recognize cardiac stun syndrome and electromechanical dissociation in patients receiving extracorporeal membrane oxygenation (ECMO), and to define patients at risk. Retrospective review. Tertiary neonatal ICU. Four newborn patients with cardiorespiratory failure who developed signs of cardiac stun syndrome and electromechanical dissociation early in the ECMO course. Initially, these patients had metabolic acidosis, chest roentgenograms showing pulmonary granularity and moderate cardiomegaly, and symptoms of severe respiratory distress. Cardiac dysfunction was apparent after ECMO was begun, with poor perfusion, pale color, narrow pulse pressure, and tachycardia despite normovolemia. Within 1 to 2 hrs, electromechanical dissociation occurred manifested by the absence of pulse pressure, palpable pulse, cardiac sounds, and apical impulse while on 50% to 70% bypass. All patients survived. Patients received ECMO, calcium gluconate, sodium bicarbonate, and dobutamine. Patients with cardiac stun syndrome have symptoms similar to severe respiratory distress syndrome, and may require ECMO support. In the ECMO patient, cardiac stun syndrome and electromechanical dissociation can be confused with low circuit volume, pneumothorax, or cardiac tamponade. Early recognition of electromechanical dissociation may improve care and outcome. Cardiac stun syndrome can be treated successfully with ECMO.

Regional vascular responses to prolonged lower body negative pressure in normal subjects.

The purpose of this study was to determine the effects of sustained unloading of baroreceptors in humans. The regional hemodynamic responses to lower body negative pressure (LBNP) were determined in 20 normal subjects. LBNP at -10 mmHg for 1 h decreased central venous pressure (CVP) without affecting blood pressure or heart rate, suggesting that only cardiopulmonary baroreceptors were unloaded. Forearm blood flow (FBF) and splanchnic blood flow (SBF) both decreased. Renal blood flow (RBF) did not change, but glomerular filtration rate (GFR) increased. Plasma renin activity rose slightly, whereas plasma norepinephrine levels did not change. Peak LBNP (either -20 or -40 mmHg for 1 h) caused a further decline in CVP and narrowed pulse pressure, thus unloading both arterial and cardiopulmonary baroreceptors. FBF returned to base-line values and SBF decreased further. RBF fell and the GFR remained increased. Plasma renin activity increased further, and plasma norepinephrine level rose. Thus the forearm and splanchnic circulations are sensitive to sustained unloading of cardiopulmonary baroreceptors; renal vasoconstriction occurs with additional unloading of arterial baroreceptors. Renin-angiotensin system activation during LBNP may be pertinent to the preservation of glomerular filtration.

Cardiac Pathology After Isolated Valve Replacement for Aortic Stenosis in Relation to Preoperative Patient Status:Early and Late Autopsy Findings

Autopsy was performed on 51 (65%) of 79 patients who underwent valve replacement for aortic stenosis in 1965-1973 and died 0 days to 14 years (mean 3.2 years) later. Heart weight index (HWI) at autopsy averaged 356 +/- 94 g/m2 and left ventricular wall thickness (LVWT) 19 +/- 4 mm. Macroscopic scattered streaky fibrosis (SSF) of the left ventricle was absent in 10% of the cases, slight in 31% and moderate/severe in 59%. Circumscript fibrotic scars were found in 31% and moderate/severe coronary artery disease (CAD) in 33%. All hearts were enlarged (HWI greater than 200 g/m2), primarily due to residual left ventricular hypertrophy (LVWT greater than 14 mm), which was present in 86% of cases. Both SSF and circumscript scars were unrelated to CAD. The preoperative predictability of autopsy findings was studied with multiple regression analyses. Predictive factors were as follows. For high HWI: high left ventricular end-diastolic pressure, short operation-autopsy time (O-A time) and high ECG hypertrophy score (ECG-hyp). For high LWT value: high cardiothoracic index (CTI), high transvalvular peak-systolic gradient and NYHA class II-III (vs. class IV). For moderate/severe SSF: high CTI and left ventricular failure. For moderate/severe CAD: short O-A time, narrow pulse pressure and low ECG-hyp. Although separated by valve replacement and a time span of up to 14 years, cardiac pathology at autopsy and preoperative patient/heart status were closely interrelated, thus emphasizing the significance of preoperatively impaired cardiac functional status and its relation to irreversible myocardial damage. The results advocate early operative intervention in aortic stenosis.

Effects of long-term clonidine administration on the hemodynamic and neuroendocrine postural responses of patients with dysautonomia.

Patients with mitral valve prolapse syndrome (MVPS), vasoregulatory asthenia, and poor postural adjustment often have orthostatic intolerance characterized by tachycardia and a narrow pulse pressure on standing. Autonomic dysfunction is thought to play an important role. Increased alpha-adrenergic activity has been shown in MVPS patients with orthostatic intolerance. We measured hemodynamic and neuroendocrine responses to long-term oral clonidine therapy in eight women, aged 36 +/- 1.8 years (27 to 44 years). None had responded favorably to beta-blockers. Heart rate, blood pressure, oxygen consumption, cardiac output, and plasma norepinephrine levels were measured in both supine and standing positions, before and after one to four weeks of clonidine (0.3 to 0.4 mg daily). Clonidine reduced standing plasma norepinephrine levels, total peripheral resistance, and diastolic blood pressure; a smaller decrease in cardiac output on standing was noted. Plasma volumes increased 12 percent. Mild reductions in plasma catecholamines and total peripheral resistance are associated with fewer, not more, orthostatic symptoms in this group of patients. "Placebo" or mild sedative effects may explain part of the response to clonidine, but the hemodynamic and neuroendocrine data suggest that decreased alpha-adrenergic hyperactivity may also be important.

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

To determine whether diabetes predisposes rats to hypertension, tail-cuff systolic pressures were measured in male rats made diabetic by pretreatment with streptozotocin. From Weeks 2 through 7, diabetic rats weighed less but had higher systolic pressures than nondiabetic ones. Further comparisons made while the rats were anesthetized with urethane showed that pressor and sympathetic nerve responses to ventromedial hypothalamic stimulation, as well as pressor responses to injected vasopressin, were significantly reduced in the diabetic group. A generalized reduction of cardiovascular reactivity was considered unlikely because systemic pressor responses to norepinephrine and tyramine were unimpaired. Yet reflex bradycardia elicited by norepinephrine was enhanced indicating that baroreceptor resetting had not occurred. Thus, diabetic rats were characterized by hypertension, narrowed pulse pressure, bradycardia with increased reflex responses to norepinephrine, and reduced pressor responses to hypothalamic stimulation and to vasopressin. The successful induction of diabetes was confirmed not only by the presence of hyperglycemia, hypoinsulinemia, glycosuria, and abnormal glucose tolerance, but also by reductions in pancreatic weight, insulin, and beta-cell content. Although our results suggest that diabetic rats are predisposed to become hypertensive, other mechanisms such as hypothalamic depression may be activated to restrict further elevations in blood pressure.

Restrictive cardiac disease. Pericarditis and the myocardiopathies

Restriction of the normal range of motion of the myocardium produces a consistent pattern of hemodynamic and clinical events. The features are similar, whether the limited cardiac action results from cardiac tamponade, constrictive pericarditis, or restrictive myocardiopathy. Persistent elevation of systemic venous pressure, prominent jugular x and y waves, and paradoxical arterial pulse may be present with any one of these disorders. Intracardiac pressures may be similar, with narrow pulse pressure in the right ventricle, an early diastolic dip in both ventricles, and approximately equal right atrial and pulmonary wedge pressures. On physical examination, evidence of right or left ventricular hypertrophy, atrial and/or ventricular gallop rhythm, or murmurs of relative mitral or tricuspid insufficiency support a diagnosis of myocardial disease rather than pericardial disease. A diagnosis of myocardiopathy is favored by an electrocardiographic pattern of bundle branch block, Wolff-Parkinson-White syndrome, or left ventricular hypertrophy. Although routine roentgen studies are often of no diagnostic value, contrast studies with cardiac radioisotope scanning, intravenous CO 2, or angiocardiography will usually permit distinction between pericardial and myocardial disease. In rare instances, the diagnostic problem cannot be resolved without resort to exploratory thoracotomy.