Low-Frequency Self-Powered Footstep Sensor Based on ZnO Nanowires on Paper Substrate.

In this work, we design and fabricate a wireless system with the main operating device based on zinc oxide (ZnO) nanowires. The main operating device is based on piezoelectric nanogenerator (NG) achieved using ZnO nanowires grown hydrothermally on paper substrate. The fabricated NG is capable of harvesting ambient mechanical energy from various kinds of human motion, e.g., footsteps. The harvested electric output has been used to serve as a self-powered pressure sensor. Without any storage device, the signal from a single footstep has successfully triggered a wireless sensor node circuit. This study demonstrates the feasibility of using ZnO nanowire piezoelectric NG as a low-frequency self-powered sensor, with potential applications in wireless sensor networks.

Risk factors for idiopathic cerebellar ataxia of late onset.

In an attempt to identify risk factors for the development of idiopathic cerebellar ataxia (IDCA) we performed a case-control study of 59 IDCA patients. Hypertension and medicine intake were less frequent in IDCA than in neurological controls. Multiple logistic regression yielded an odds ratio (OR) for hypertension of 0.13 (95% confidence interval: 0.00-1.02, P=0.0527) and medicine intake of 0.10 (95% confidence interval: 0.00-0.72, P=0.0157). In contrast, we did not identify an association of IDCA with a number of medical diseases, head trauma, smoking, alcohol intake, rural living and well-water drinking. Some of these factors have been previously shown to be associated with other neurodegenerative diseases. In addition, serum antibody titers against neurotropic viruses were not elevated in IDCA.

The hemodynamic and clinical responses to terazosin, a new alpha blocking agent, in congestive heart failure.

To determine the hemodynamic effects of a new alpha 1 blocker, terazosin, in congestive heart failure, six patients with this condition underwent hemodynamic testing (at rest and during exercise) before and after dosing. Doses of 2, 5, and 10 mg were examined in sequence over 3 days to define dose-response characteristics. Terazosin, in these doses, decreased pulmonary and systemic vascular resistances and right atrial and pulmonary capillary wedge pressures. Terazosin increased stroke volume and cardiac output, presumably through afterload-reduction, without altering heart rate. These aforementioned responses were apparent both at rest and during exercise. While a direct relationship existed between dose and plasma concentration, a similar relationship was not observed for dose (or plasma concentration) and hemodynamic response; no differences were noted between the hemodynamic responses to the three doses. Improvement in hemodynamics persisted and the clinical status and exercise capacity improved in the four patients chronically treated (over 2 months) with terazosin. Treating the heightened tone of the sympathetic nervous system in congestive heart failure with the alpha 1 blocker, terazosin, may be of benefit to some patients afflicted with this disorder.

The hemodynamic effects of ibopamine, a dopamine congener, in patients with congestive heart failure.

Ten patients with congestive heart failure underwent noninvasive and invasive hemodynamic testing before and sequentially after the administration of ibopamine to determine the cardiovascular effects of this oral dopamine congener. Single doses of 200, 400 and 600 mg were administered to all patients and 5 repeated doses of 200 or 400 mg were studied in 8. Hemodynamic effects occurred as early as 30 minutes and lasted up to 4 hours after dosing. In general, ibopamine elicited statistically significant dose-related increases in cardiac output and reductions in the derived resistance of the systemic and pulmonary circulations. A biphasic response in central and peripheral pressures was observed; up to 1 hour after administration, ibopamine elevated mean right and left atrial pressures and pulmonary and systemic arterial pressures with a significant reduction of these measurements beyond 1 hour. It did not alter heart rate. Repeated doses qualitatively affected hemodynamics similar to the initial dose and did not appear to be accompanied by short-term tolerance. While oral ibopamine elicits some favorable hemodynamic effects in humans with cardiac failure, the biphasic hemodynamic response is generally undesirable in the majority of these patients.

Preliminary observations of chronic indoramin therapy in congestive heart failure.

Twenty-one patients with congestive heart failure (New York Heart Association functional class III) underwent a double-blind, parallel, placebo-controlled, randomized trial of indoramin (average dose of 50 mg every 12 h in 11 patients) versus placebo (n = 10). The study lasted 2 months and was initiated and terminated with the measurement of resting and exercise hemodynamics. Compared with baseline values, chronic administration of indoramin caused a mild reduction in resting mean systemic blood pressure (mean change of -10 mm Hg), and postdosing results included a drop in systemic and pulmonary vascular resistances and pulmonary capillary wedge pressure and a mild increase in stroke volume. Compared with baseline responses, chronic indoramin administration (postdosing) elicited a mild reduction in systemic and pulmonary vascular resistances and pulmonary capillary wedge pressure during submaximal exercise. At this dose, chronic indoramin administration did not alter hemodynamics at maximal exercise or exercise duration to maximal exercise. While certain individual patients experienced clinical improvement on chronic indoramin therapy, the overall clinical status (symptoms, signs, diuretic requirements) of the indoramin-treated group did not change significantly when compared with that of the placebo control group.

Nifedipine in congestive heart failure: effects on resting and exercise hemodynamics and regional blood flow.

Ten patients with moderate to severe congestive heart failure (CHF) underwent central and regional hemodynamic measurements at rest and central hemodynamic measurements during exercise before and after the oral administration of nifedipine (0.2 mg/kg). Nifedipine significantly decreased systemic blood pressure, systemic vascular resistance, pulmonary artery pressure, pulmonary vascular resistance, and pulmonary capillary wedge pressure. Stroke volume and cardiac output increased after nifedipine. The measured parameters of left ventricular inotropy did not change significantly for this calcium channel blocker. While blood flow to renal, hepatic, and limb vascular beds increased (p less than 0.05 for renal and limb) after nifedipine, only limb blood flow increased in proportion to the increase in cardiac output, suggesting preferential dilatation of limb vasculature. Although initial-dose nifedipine did not increase exercise duration, it elicited an improvement in exercise hemodynamics by reducing systemic vascular resistance and pulmonary capillary wedge pressure and increasing stroke volume and cardiac output. The calcium channel blocker, nifedipine, can be administered safely in the setting of ventricular failure and appears to favorably alter resting and exercise hemodynamics. A select number of patients with CHF may benefit from its long-term administration.

Chronic oral amrinone therapy in congestive heart failure: a double-blind placebo-controlled withdrawal study.

Eighteen patients with congestive heart failure were studied in a double-blind, randomized, placebo-controlled withdrawal trial to evaluate the effectiveness of chronic oral amrinone therapy when added to conventional heart failure therapy. All patients received a four-week lead-in of amrinone 100 mg orally every 8 h, then were randomly assigned to either continued amrinone (nine patients) or placebo (nine patients) groups. Compared to placebo, chronic amrinone therapy did not significantly improve clinical status, left ventricular function as measured by non-invasive testing techniques, or exercise tolerance. Side-effects occurred in every patient receiving amrinone and abated in those patients who received placebo for the last 12 weeks of the study. The limited effectiveness of oral amrinone and the high frequency of side-effects preclude the widespread use of this drug in the chronic therapy of congestive heart failure.

Amrinone therapy for congestive heart failure in outpatients with idiopathic dilated cardiomyopathy.

Amrinone, 100 mg orally every 8 hours, was administered to 13 patients with moderate-to-severe congestive heart failure (CHF) for 1 month on an outpatient basis to determine the beneficial and undesirable effects of this new cardioactive agent in this clinical setting. These subjects received conventional CHF medications during the course of study. Ten patients who received conventional CHF medications alone served as a control group. Changes in functional classification were not significantly different between the 2 treatment groups. Amrinone augmented exercise capacity 37% above baseline compared with a 12% improvement for the control group. Noninvasive indexes of resting left ventricular function (echocardiography and systolic time intervals) did not change significantly for either group, nor was there a significant change in the exercise ejection fraction. All patients treated with amrinone had greater than or equal to 1 symptom-related or laboratory-detected adverse effect. An increase in the frequency of ventricular ectopic beats was noted at rest in 4 and with exercise in 6 patients (salvos of nonsustained ventricular tachycardia in 2). Six subjects treated with amrinone had gastrointestinal symptoms and 8 developed a viral-like illness. Other adverse effects noted in the amrinone-treated group included near-syncope, headaches, marked anxiety, chest pain, palpitations, maculopapular rash, hypokalemia, and elevation of serum transaminase levels. The control patients had significantly fewer adverse effects. Although individual patients with CHF may benefit from long-term amrinone therapy, the low benefit-to-risk-adverse effect ratio does not warrant widespread application of this drug in the outpatient management of CHF and requires caution when prescribing.

Improved exercise capacity and differing arterial and venous tolerance during chronic isosorbide dinitrate therapy for congestive heart failure.

We studied 30 patients with moderate-to-severe congestive heart failure in a double-blind, randomized, placebo-controlled trial to determine the acute and long-term effects of isosorbide dinitrate on clinical status and on resting and exercise hemodynamics. Seventeen patients received placebo and 13 isosorbide dinitrate. First-dose isosorbide dinitrate (40 mg orally) decreased resting and exercise pulmonary capillary wedge pressure, pulmonic and systemic arterial pressures and pulmonic and systemic vascular resistances without augmenting exercise capacity. Compared with placebo, chronic therapy with isosorbide dinitrate (40 mg orally every 6 hours for 12 weeks) significantly improved clinical status and exercise capacity. Resting and exercise systemic blood pressure and systemic vascular resistance returned to baseline values during chronic isosorbide dinitrate therapy, but pulmonary capillary wedge pressure, pulmonary artery pressure and pulmonary vascular resistance remained improved. In patients with congestive heart failure, 12 weeks of oral isosorbide dinitrate therapy improves resting and exercise hemodynamics, exercise capacity, and clinical status; tolerance develops to the systemic arterial vascular effects without attenuation of the venous and pulmonary vascular effects.

Captopril in primary pulmonary hypertension.

Seven women with primary pulmonary hypertension underwent hemodynamic evaluation, at rest and during exercise, before and after the oral administration of captopril. Dose-response curves were generated for the 25-, 50- and 100-mg doses. Captopril significantly reduced systemic blood pressure and systemic vascular resistance; these effects persisted at submaximal levels of exercise. Captopril did not alter pulmonary artery pressure or resistance, cardiac output or stroke volume at rest or during exercise. Exercise tolerance did not improve. Four of the patients also received captopril chronically for 12 weeks at doses of 75 and 100 mg every 8 hours. Resting and exercise hemodynamic evaluation was repeated at the end of the 12-week period. Except for a persistent reduction in mean systemic blood pressure at rest, chronic captopril administration did not elicit hemodynamic changes. Measured exercise duration did not change during continuous captopril treatment, although one patient reported mild subjective improvement in activity tolerance. In primary pulmonary hypertension, captopril exerts its major effect on systemic vasculature, with little or no effect on the pulmonary circuit. While an occasional patient may experience some clinical improvement with captopril therapy, the majority of adult patients with severe primary pulmonary hypertension will not benefit from its chronic administration.

Acute and chronic isosorbide dinitrate therapy in congestive heart failure: demonstration of improved exercise capacity and differing arterial and venous tolerance during chronic administration.

Thirty patients with congestive heart failure underwent a double-blind study after randomization into either isosorbide dinitrate or placebo. The initial dose (40 mg orally) of isosorbide dinitrate reduced resting and exercise pulmonary artery, pulmonary capillary wedge, and systemic blood pressure and pulmonary and systemic vascular resistance without improving exercise tolerance. Chronic dosing (40 mg orally every 6 h for 3 months) increased exercise tolerance and maintained a reduction in resting and exercise pulmonary artery and pulmonary capillary wedge pressures and pulmonary resistance, while systemic pressure and resistance returned to baseline. Chronic oral isosorbide dinitrate (40 mg every 6 h) improves exercise capacity over a 3-month period with disparate tolerance effects on systemic arterial, systemic venous, and pulmonary vasculature.

Vasodilators and prostaglandin inhibitors in primary pulmonary hypertension.

Ten women with primary pulmonary hypertension had resting hemodynamic measurements taken before and after the nonparenteral administration of various vasodilators and prostaglandin inhibitors. Only sublingual isoproterenol, alone or combined with sublingual isosorbide dinitrate, effected a substantial (greater than 20%) drop in pulmonary vascular resistance; this decrease was accompanied by little change in pulmonary artery pressure. Isosorbide dinitrate was the only drug that elicited any reduction in pulmonary artery pressure; pulmonary vascular resistance decreased modestly. The oral administration of diazoxide, hydralazine, phentolamine, and tolazoline elicited little change in pulmonary artery pressure or resistance. Except for tolazoline, all these agents significantly decreased systemic blood pressure and resistance. Prostaglandin inhibition by indomethacin (acute and chronic dosing) increased pulmonary and systemic vascular resistances and reduced cardiac output. Aspirin combined with dipyridamole elicited no changes. The vasodilators and prostaglandin inhibitors studied evoked little improvement in resting pulmonary hemodynamic abnormalities in primary pulmonary hypertension.

Drug-induced conditioning in congestive heart failure.

Continuous 72-hour infusions of dobutamine reportedly effect sustained clinical improvement in patients with congestive heart failure. This study was designed to determine if shorter, more frequent infusions, delivered in an outpatient setting, elicit a similar response. Twenty-six patients with moderately severe congestive heart failure were randomized, 11 into a control group and 15 into a dobutamine treatment group. Baseline data were collected for 4 weeks in each group. Thereafter, the dobutamine treatment group received 4-hour infusions of dobutamine weekly for 24 weeks. Systolic time intervals, echocardiography, cardiac index and treadmill exercise tolerance were used to follow the progress of the control and dobutamine treatment groups. The ratio of preejection period to left ventricular ejection time and the cardiac index did not change significantly in either group. The velocity of circumferential fiber shortening and the percent change in the minor axis of the left ventricle during systole improved modestly (p less than 0.05) above baseline in the dobutamine group after 14 weeks of treatment and above the corresponding control values (p less than 0.05) after 22 weeks. Exercise tolerance (duration) improved 25--51% (all p less than 0.05) above baseline in the dobutamine group compared with 10--17% (all p greater than 0.05 vs baseline) in the control group. Heart rate at maximal exercise did not change significantly from baseline for either group and did not differ significantly between the two groups. Functional classification improved in 12 of 15 dobutamine treatment patients and in only two of 11 control patients (p less than 0.05). In our patients with congestive heart failure, weekly 4-hour dobutamine infusions did not elicit a major change in resting left ventricular function; however, exercise performance and clinical status improved considerably.

Intravenous pirbuterol.

Pirbuterol was given intravenously to nine normal men to determine the hemodynamic effects of intravenous injection of this rather selective beta 2-adrenoceptor agonist. Pirbuterol induced marked improvement of the echocardiographic (percent change in the dimension of the minor axis of the left ventricle during systole, ejection fraction, and velocity of left ventricular circumferential fiber shortening) and systolic time interval (preejection period interval, preejection period/left ventricular ejection time) indices of ventricular performance. The increase in stroke volume was indicated by elevation of systolic blood pressure and widening of pulse pressure. Vascular beta 2-receptor agonist effects were indicated by the fall in diastolic and mean systemic blood pressure and marked reduction in derived systemic vascular resistance. Dose-related positive chronotropic properties were observed without dysrhythmias. There was a good direct correlation between mean plasma pirbuterol concentration and dose. Because of the reported efficacy of oral doses, the direct relationship between plasma concentration and dosage, the positive inotropic properties, and the peripheral vasodilating effects of pirbuterol, investigation of the intravenous form of the drug in patients with severe decompensated low-output congestive heart failure seems warranted.

Hemodynamic effects of intravenous butopamine in congestive heart failure.

Butopamine is chemically similar to dobutamine but, unlike dobutamine, it is not a catecholamine. Preclinical studies on dogs show that butopamine is inotropic intravenously and orally. We gave butopamine intravenously to eight patients with congestive heart failure using a progressive dose-response protocol ranging from 0.02 to 0.17 mcg/kg/min. The mean cardiac index and stroke volume index increased at doses greater than or equal to 0.06 mcg/kg/min; there was also an increase in heart rate at greater than or equal to 0.06 mcg/kg/min. At greater than or equal to 0.08 mcg/kg/min the augmented stroke volume tended to plateau so that additional increases in the cardiac index were secondary to the elevated heart rate. Improved ventricular performance, measured by systolic time intervals, left ventricular stroke work index, and the calculated mean rate of left ventricular pressure development during isovolumetric contraction (delta P/delta t/PCWP), was noted at greater than or equal to 0.06 mcg/kg/min. Systemic systolic blood pressure increased at greater than or equal to 0.04 mcg/kg/min but diastolic and mean arterial pressures and pulmonary artery and pulmonary capillary wedge pressures did not change. The progressive increase in cardiac output was accompanied by a reduction in pulmonary and systemic vascular resistances. Although mean premature ventricular contractions per minute did not change, two patients experienced a substantial increase in ventricular ectopy at 0.10 and 0.12 mcg/kg/min. Butopamine induces a positive inotropic response in patients with congestive heart failure but for equal increments in cardiac output, butopamine increases heart rate more than dobutamine.

Comparative systemic and regional hemodynamic effects of dopamine and dobutamine in patients with cardiomyopathic heart failure.

Thirteen patients with severe cardiac failure underwent a single crossover study of dopamine and dobutamine in order to compare the systemic and regional hemodynamic effects of the two drugs. The dose-response data demonstrated that dobutamine (2.5--10 microgram/kg/min) progressively and predictably increases cardiac output by increasing stroke volume, while simultaneously decreasing systemic and pulmonary vascular resistance and pulmonary capillary wedge pressure. There was no change in heart rate or premature ventricular contractions (PVCs)/min at this dose range. Dopamine (2--8 microgram/kg/min) increased the stroke volume and cardiac output at 4 microgram/kg/min. Dopamine at less than 4 microgram/kg/min provided little additional increase in cardiac output and increased the pulmonary wedge pressure and the number of PVCs/min. At greater than 6 microgram/kg/min, dopamine increased heart rate. During the 24-hour maintenance-dose infusion of each drug (dopamine 3.7--4, dobutamine 7.3--7.7 microgram/kg/min), only dobutamine maintained a significant increase of stroke volume, cardiac output, urine flow, urine sodium concentration, creatinine clearance and peripheral blood flow. Renal and hepatic blood flow were not signfiicantly altered by the maintenance dose of either drug. Systemic and regional hemodynamic data suggest that dobutamine has many advantages over dopamine when infused in patients with cardiac failure.

Complex atrial dysrhythmias in a patient with congestive cardiomyopathy.

A patient with primary cardiomyopathy and long standing atrial fibrillation presented with atrial tachycardia and AV block. Atrial pacing sequentially converted the atrial tachycardia to atrial flutter (biatrial) and to the dissimilar atrial rhythms of right atrial fibrillation with left atrial flutter, right atrial flutter with left atrial electrical standstill and right atrial fibrillation with left atrial standstill. The clincial milieu and intracardiac recordings are presented.