Biomedical subjects
Publications and source records attributed to A H Nguyen.
Complications associated with coronary stent placement have decreased in recent years. One of the complications involved with this procedure is the possibility that the stent is stripped from the delivery catheter prior to deployment and is lost systemically. This paper reports a rare complication which resulted in vascular insufficiency necessitating surgical intervention.
The mere recognition of cardiac failure should not be the sole diagnostic aim. Diagnosis must also include the search for the underlying cause of cardiac failure and for its precipitating causes, as well as the assessment of its severity. Each step is essential because it contributes to the choice of an appropriate treatment. Full diagnosis take into account disease history, physical examination, electrocardiogram and chest X-ray; in addition, informations provided by cardiac echography play an increasing role in the assessment of cardiac failure.
BACKGROUND: Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impact of triggers on sympathetic nerve activity and regional blood flow in heart failure has not been examined in patients with heart failure. METHODS AND RESULTS: Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects. CONCLUSIONS: Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest.
During static exercise, several reflex systems that increase sympathetic nerve activity, heart rate, arterial pressure, and cardiac output are activated. At rest, the renal circulation receives the most blood flow per tissue weight of any organ in the body. However, the renal circulatory response to static exercise has not been studied in humans because of technical limitations in methods for measuring rapid changes in renal blood flow. The aim of this study was to determine the renal blood flow response to static exercise in healthy humans and, specifically, to clarify the reflex mechanisms underlying this response. Renal cortical blood flow was measured using dynamic positron emission tomography and the blood flow agent oxygen-15 water. Graded handgrip exercise, posthandgrip circulatory arrest, and administration of intra-arterial adenosine were performed to clarify the mechanisms controlling renal blood flow during static exercise. The major new findings in this study are that in healthy humans (1) renal cortical blood flow decreases (basal versus handgrip, 4.4 +/- 0.1 versus 3.5 +/- 0.1 mL.min-1.g-1; P = .008) and renal cortical vascular resistance increases (basal versus handgrip, 17 +/- 1 versus 26 +/- 2 U; P = .01) in response to static handgrip exercise; (2) central command and/or the mechanoreflex contributes importantly to the early decrease in renal blood flow (basal versus handgrip, 4.2 +/- 0.2 versus 3.5 +/- 0.3 mL.min-1.g-1; P = .04) and to the increase in renal cortical vascular resistance (basal versus handgrip, 20 +/- 1 versus 25 +/- 2 U; P = .04); (3) the muscle metaboreflex contributes to further decreases in renal blood flow (basal versus posthandgrip circulatory arrest, 4.3 +/- 0.1 versus 3.5 +/- 0.2 mL.min-1.g-1; P = .002) and increases in renal cortical vascular resistance (basal versus handgrip, 18 +/- 1 versus 25 +/- 3 U; P = .002); and (4) exogenous adenosine activates the muscle metaboreflex producing reflex renal vasoconstriction and decreased renal blood flow, which may implicate endogenous adenosine generated during ischemic exercise as a potential activator of the muscle metaboreflex during ischemic handgrip exercise.
Muscle sympathetic nerve activity (MSNA) is increased in patients with heart failure compared with healthy subjects. We applied spectral and correlation techniques to determine if qualitative as well as quantitative differences in MSNA differentiate heart failure patients from healthy subjects. We recorded MSNA, heart rate, and respiration in 11 heart failure patients and 10 healthy humans. Our results are as follows. 1) Statistically significant low-frequency modulation of MSNA at 0.029 +/- 0.002 Hz (mean +/- SE; range 0.026-0.038 Hz) was found in 10 of 11 heart failure patients but in only 2 of 10 healthy controls (differences between groups, P < 0.01; chi 2 test). 2) Heart rate and respiration also demonstrated significant low-frequency modulation in a similar range. 3) Spectral and correlation techniques revealed that low-frequency modulation of MSNA was highly correlated with low-frequency modulation of respiration in heart failure patients, but not in healthy subjects. In contrast, low-frequency modulation of MSNA did not correlate well with low-frequency modulation of heart rate. In summary, low-frequency modulation of respiration is coupled to low-frequency modulation of MSNA in heart failure patients, but not in normal subjects. We speculate that this low-frequency modulation of respiration may represent subclinical Cheyne-Stokes breathing, which has marked qualitative effects on MSNA in patients with heart failure.
PURPOSE: This study was designed to measure the effect of intermittent pneumatic compression of the plantar venous plexus on popliteal vein (PV) and common femoral vein (CFV) velocities measured by duplex ultrasound scanning. METHODS: Thirty lower limbs in 15 healthy volunteers had venous duplex scanning measurement of PV and CFV velocities before and during foot pumping with an arteriovenous impulse foot pump system. Venous velocities were measured at two pump pressure settings (100 mm Hg, 200 mm Hg) and during two pump impulse durations (short = 1 second, normal = 3 seconds). All limbs were examined with the subjects in the supine position, and then measurements were repeated with subjects in the 15-degree reverse Trendelenburg position. The mean maximum venous velocity (MVV) produced by foot pumping was compared with resting venous velocity at each anatomic location and for each technologic variable. RESULTS: Impulse foot pumping produced a statistically significant increase in MVV in both the PV and the CFV compared with resting velocities. This significant increase was observed for both pressure settings and both impulse durations, and no differences produced by these two individual variables could be detected. The increase in MVV produced by foot pumping was similar for limbs in the supine position and those examined in the reverse Trendelenburg position. The percentage increase in MVV produced by foot pumping was significantly higher in the PV than in the CFV. CONCLUSIONS: Intermittent pneumatic compression of the plantar venous plexus produces measurable increases in venous outflow from the lower limbs of normal subjects. This study seems to justify further evaluation of the effectiveness of this technique for mechanical deep venous thrombosis prophylaxis in selected high-risk patient groups.
The DNA of the Bacillus subtilis temperate phage phi 3T is not susceptible to cleavage by the restriction endonuclease HaeIII, although it is cut by many other restriction enzymes. The host DNA from uninfected cells is cut by HaeIII. We show that phi 3T DNA propagated in a restriction-modification-defective Escherichia coli cell can be digested by HaeIII. Thus, phi 3T DNA does contain the nucleotide recognition sequence of HaeIII. We suggest that this phage induces the modification of its own DNA. In support of this mechanism we show that extracts prepared from phi 3T-infected cells contain an activity which in the presence of S-adenosyl-L-methionine (SAM) can modify lambda DNA against cleavage by HaeIII. The same in vitro-modified DNA is still susceptible to cleavage by other restriction endonucleases.
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Smart instruments require on-line computers, special purpose hardware, or both. A pupillometer is described that relies only on a general purpose microcomputer with a frame grabber to process infrared video camera pictures of the human eye. An essential feature of the instrument is that a top-down model controls the image processing algorithms. The model generates regions of interest, ROIs, positioned from knowledge of anatomy and optics of the eye and information from previously analyzed frames. Within these adaptively controlled ROIs, fast, run-time algorithms automatically calculate local thresholds, area measurements, moments for centroid position information, and use pyramiding to shorten calculation time for large pupils. Outputs are precise measurements of pupil size and eye position in real time, with adequate bandwidth for most purposes.