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Biomedical subjects

J L Houghton

Publications and source records attributed to J L Houghton.

At least 19 recordsLinked to original sources
PubMed2007

Continuous enrichment culturing of thermophiles under sulfate and nitrate-reducing conditions and at deep-sea hydrostatic pressures.

A continuous culture bioreactor was developed to enrich for nitrate and sulfate reducing thermophiles under in situ deep-sea pressures. The ultimate objective of this experimental design was to be able to study microbial activities at chemical and physical conditions relevant to seafloor hydrothermal vents. Sulfide, sulfate and oxide minerals from sampled seafloor vent-chimney structures [East Pacific Rise (9 degrees 46'N)] served as source mineral and microbial inoculum for enrichment culturing using nitrate and sulfate-enriched media at 70 and 90 degrees C and 250 bars. Changes in microbial diversity during the continuous reaction flow were monitored using denaturing gradient gel electrophoresis (DGGE) of PCR amplified 16S rRNA gene fragments. Time series changes in fluid chemistry were also monitored throughout the experiment to assess the feedback between mineral-fluid reaction and metabolic processes. Data indicate a shift from the dominance of epsilon Proteobacteria in the initial inoculum to the several Aquificales-like phylotypes in nitrate-reducing enrichment media and Thermodesulfobacteriales in the sulfate-reducing enrichment media. Methanogens were detected in the original sulfide sample and grew in selected sulfate-enriched experiments. Microbial interactions with anhydrite and pyrrhotite in the chimney material resulted in measurable changes in fluid chemistry despite a fluid residence time only 75 min in the reactor. Changes in temperature rather than source material resulted in greater differences in microbial enrichments and mediated geochemical reactions.

Biodiversity↗
PubMed2000

Cholesterol lowering with pravastatin improves resistance artery endothelial function: report of six subjects with normal coronary arteriograms.

STUDY OBJECTIVES: Improvement in coronary artery endothelial function has been demonstrated after cholesterol lowering in hypercholesterolemic patients with significant atherosclerosis. However, to our knowledge, no previous study has shown improvement in resistance artery function in subjects with normal coronary arteries after cholesterol lowering. The purpose of our study was to investigate the effect of cholesterol lowering with pravastatin on coronary resistance artery endothelial function in the setting of angiographically normal coronary arteries. METHODS: Invasive testing of coronary endothelial and vasomotor function was performed at baseline and after 6 months of pravastatin treatment in six patients with normal coronary arteriograms. RESULTS: After 6 months of pravastatin treatment, low-density lipoprotein cholesterol level dropped from 157+/-11 to 117+/-8 mg/dL (p = 0.02) and percent increase in coronary blood flow after acetylcholine improved from 97+/-13% to 160+/-16% (p = 0.01). There was a trend (p = 0.17) toward enhanced epicardial dilation in response to acetylcholine after pravastatin treatment when compared with the baseline study. CONCLUSIONS: Our study demonstrates significant improvement in coronary resistance artery endothelial function after 6 months of cholesterol lowering with pravastatin in six subjects presenting with chest pain who were found to have normal coronary arteriograms. A trend toward improved epicardial vasomotion was also observed.

Adult↗
PubMed2000

Basal and reserve renal artery blood flow: effect of endothelium-dependent and -independent vasoactive agonists and radiographic contrast medium in two patients.

This manuscript describes the results of invasive testing of renal artery and arteriolar reactivity in two patients using a panel of endothelium-dependent and -independent agents including radiographic contrast medium. We found that the renal artery and microcirculation dilate in response to graded acetylcholine infusions and to bolus nitroglycerin infusion; the renal microcirculation dilates in response to papaverine but constricts after adenosine and after radiographic contrast medium. Future indications for this testing are briefly discussed.

Acetylcholine↗
PubMed1999

Spontaneous multivessel coronary artery dissection: repeated presentation in a healthy postmenopausal woman.

Spontaneous coronary artery dissection is a rare cause of acute myocardial infarction which is infrequently diagnosed antemortem. Most previously reported cases were found in women of whom a significant proportion presented during pregnancy or the postpartum period. We describe the first antemortem case of spontaneous coronary artery dissection, unrelated to pregnancy or the postpartum state, which ultimately resulted in diffuse involvement of both the left and right coronary arteries over a period of 4 months. Pathophysiology and case management of this disorder are discussed.

Adult↗
PubMed1998

Heterogeneous vasomotor responses of coronary conduit and resistance vessels in hypertension.

OBJECTIVES: The purpose of our study was to investigate the relation between conductance and resistance coronary vasomotor responsiveness in hypertensive patients without atherosclerosis. BACKGROUND: Although similar in morphology, conduit and resistance coronary vessels differ importantly in size, function and local environment and appear to be differentially affected in certain disease processes, such as atherosclerosis and hypertension. However, little is known about the effect of hypertension on contiguous coronary conduit and resistance vessels in humans. METHODS: Changes in coronary blood flow (a measure of resistance vessel reactivity) and coronary artery diameter (a measure of conduit vessel reactivity) were investigated in response to graded infusion of the endothelium-dependent agonist acetylcholine (ACh) in 98 patients with normal coronary arteries. RESULTS: In 31 normotensive, euglycemic patients, conduit and resistance coronary artery responses to intracoronary infusion of ACh were significantly correlated (r = 0.73, p = 1 x 10[-6]), although eight patients (26%) had constriction of conduit but dilation of resistance arteries at peak effect. In 28 hypertensive patients without left ventricular hypertrophy (LVH), conduit and resistance artery responses to ACh remained significantly correlated (r = 0.5, p = 0.006), although 12 patients (43%) had discordant findings. Finally, in 39 hypertensive patients with LVH, conduit and resistance artery responses to ACh displayed the lowest correlation (r = 0.38, p = 0.02), with 22 patients (56%) demonstrating conduit artery constriction and resistance artery dilation. CONCLUSIONS: Despite angiographically normal coronary arteries, heterogeneous vasomotor responses (dilation and constriction) were demonstrated in contiguous conduit and resistance arteries in normotensive and hypertensive patients referred for cardiac catheterization because of chest pain. In addition to more severe endothelial dysfunction among conduit and resistance arteries, a greater frequency of discordant conduit and resistance artery responses and resistance vessel constriction was found with increasing severity of hypertension. Our study suggests differing mechanisms of endothelium responsiveness to ACh among conduit and resistance coronary arteries.

Acetylcholine↗
PubMed1997

Coronary vasomotor reactivity among normotensive African and white American subjects with chest pain.

BACKGROUND AND OBJECTIVES: Excess cardiovascular morbidity and mortality among African (black) Americans is the subject of intensive investigation but the etiology remains speculative. One hypothesis proposes that inherent, or intrinsic, differences in coronary vascular reactivity and endothelial function predispose African Americans to enhanced vasoconstriction and/or depressed vasodilation, resulting in excess ischemia. The objective of this study was to establish whether coronary vasoreactivity differs among normotensive, nondiabetic African and white Americans with normal arteries referred for coronary arteriography because of chest pain. PATIENTS AND METHODS: Eleven African American (8 female, 3 male) and 28 white American (9 female, 19 male) normotensive, euglycemic patients with normal coronary arteries were prospectively recruited for invasive testing of coronary artery and microvascular relaxation using the endothelium-dependent and -independent agents, acetylcholine and adenosine; a Doppler tipped intracoronary guidewire; and quantitative coronary angiography. RESULTS: The study cohort consisted of 17 women (44%) and 22 men (56%) with a mean age of 46 +/- 10 yrs. Of 8 African American women, 6 were premenopausal and 2 were postmenopausal on estrogen replacement therapy. Of 9 white American women, 2 were premenopausal, 1 was 46-year old with a previous history of hysterectomy without ovariectomy, 2 were postmenopausal on estrogen replacement therapy, 2 were perimenopausal and 44- and 54-year old, and 2 were postmenopausal without estrogen replacement therapy. In response to maximal infusion of acetylcholine, epicardial coronary arteries and resistance vessels dilated similarly in black and white subjects. Dose-response curves revealed no significant racial differences during submaximal graded infusion of acetylcholine. In response to peak effect of adenosine, there were no racial differences in dilation of the microcirculation. CONCLUSIONS: In the absence of hypertension, diabetes mellitus, and angiographic evidence of coronary artery disease, African American women demonstrate no evidence of intrinsic predisposition to enhanced coronary conduit vasoconstriction or depressed microcirculatory dilation in response to the endothelium-dependent and -independent vasodilator agonists-acetylcholine and adenosine-when compared with responses of similar white men and women. Because of low enrollment of black males, definitive conclusions cannot be drawn regarding this group.

Adult↗
PubMed1997

Effect of African-American race and hypertensive left ventricular hypertrophy on coronary vascular reactivity and endothelial function.

Excess cardiovascular morbidity and mortality among African (black) Americans remains an important yet unexplained public health problem. One possible explanation proposes that intrinsic or acquired abnormalities in coronary vascular reactivity and endothelial function result in excess ischemia among black Americans. To examine this hypothesis, we subjected 80 individuals with normal coronary arteries to invasive testing of coronary artery and microvascular relaxation using intracoronary infusions of acetylcholine and adenosine, a Doppler tipped intracoronary guide wire, and quantitative coronary angiography. We measured the percent increase in coronary blood flow and epicardial diameter after graded infusion of intracoronary acetylcholine and in coronary blood flow after intracoronary adenosine in 31 normotensive subjects (10 black, 21 white) and 49 hypertensive subjects with left ventricular hypertrophy (25 black, 24 white). Categorical and multivariate analyses revealed that in response to intracoronary adenosine and acetylcholine, the depression in endothelium-independent and -dependent microvascular relaxation during peak agonist effect was largely related to the presence of chronic hypertension and left ventricular hypertrophy. Normotensive subjects demonstrated no intrinsic racial differences in conduit and resistance vessel vasoreactivity. In response to maximal infusion of acetylcholine, epicardial coronary arteries constricted similarly in black and white subjects with hypertensive left ventricular hypertrophy and dilated similarly in normotensive black and white subjects. Thus, our study shows that in a cohort of black and white subjects referred for coronary arteriography because of chest pain, African American race is not associated with excess intrinsic or acquired depression in coronary vascular relaxation during the peak effect of the endothelium-dependent and -independent agonists acetylcholine and adenosine, after adjustment for the presence of left ventricular hypertrophy.

Adenosine↗
PubMed1996

Coronary vasomotor function in a normotensive, nondiabetic referral population with normal coronary arteriograms.

In a referral normal cardiac population, endothelium-independent coronary relaxation is nearly always normal, but endothelium-dependent relaxation may be depressed in a significant proportion of patients. Further study of the natural history of referral subjects with endothelial dysfunction is necessary to assess the potential cardiovascular risk of this finding in a presumed low-risk population.

Acetylcholine↗
PubMed1994

Hypertensive heart disease. How does blood pressure affect left ventricular mass?

Currently, echocardiography is the most accepted tool for diagnosing the left ventricular hypertrophy that characterizes hypertensive heart disease; electrocardiography is not adequately sensitive. The symptoms and signs of coronary artery disease (CAD) and of hypertensive heart disease are similar and include angina, myocardial infarction, systolic and diastolic heart failure, atrial fibrillation, ventricular ectopy, and sudden death. Thallium stress testing is useful for excluding significant CAD; a positive test requires cardiac catheterization to eliminate large-vessel disease as the cause of myocardial ischemia. Regression of left ventricular hypertrophy is a treatment goal.

Coronary Disease↗
PubMed1994

Racial differences in myocardial ischemia and coronary flow reserve in hypertension.

OBJECTIVES: Using invasive measurements of endothelium-independent coronary flow reserve and stress thallium testing with or without dipyridamole, this study investigated racial differences in ischemia and coronary reserve in hypertensive left ventricular hypertrophy. BACKGROUND: African Americans compared with Caucasian Americans appear to have a higher case fatality from coronary heart disease but lesser amounts of atherosclerotic coronary artery disease. This paradox may be explainable by intrinsic or acquired racial differences in coronary arteriolar autoregulation and vasoreactivity. METHODS: The study enrolled 91 African and 81 Caucasian Americans referred for cardiac catheterization because of suspected myocardial ischemia but found to have no significant coronary stenosis. Patients were stratified by degree of left ventricular hypertrophy for comparison purposes after calculation of indexed left ventricular mass by means of echocardiographic M-mode measurements. Coronary flow reserve measurements were made using the intracoronary Doppler catheter and hyperemic doses of intravenous dipyridamole in 100 patients and intracoronary papaverine and adenosine in 72 patients. Seventy-seven percent of patients underwent adequate stress thallium testing with or without dipyridamole. RESULTS: In African Americans, mean (+/- SD) coronary flow reserve decreased from 4.4 +/- 2.3 for 38 without mass hypertrophy to 3.2 +/- 1.3 for 53 with hypertrophy (p = 0.005) to 2.7 +/- 1.1 for 12 with severe hypertrophy (p = 0.02). Thallium testing was abnormal in 31% of those without mass hypertrophy and 59% of those with hypertrophy. In Caucasian Americans, coronary flow reserve decreased from 4.1 +/- 2 for 58 without hypertrophy to 3.6 +/- 1.5 for 23 with hypertrophy (p = NS) to 3 +/- 1.5 for 6 with severe hypertrophy (p = NS). Thallium testing was abnormal in 36% without mass hypertrophy and in 39% with hypertrophy. CONCLUSIONS: This study establishes that development of left ventricular hypertrophy in hypertension carries greater physiologic morbidity for African compared with Caucasian Americans, typified by marked reduction in endothelium-independent coronary flow reserve and increased frequency of abnormal thallium tests.

Aged↗
PubMed1994

Unstable angina. Pharmaceutical versus invasive therapy.

Because unstable angina is often a precursor of myocardial infarction or death, patients with chest pain that persists for more than 20 minutes and is refractory to sublingual nitroglycerin should be hospitalized in an intensive care unit and given appropriate pharmacologic therapy. If symptoms persist despite adequate management with drugs, coronary arteriography should be performed and consideration given to an invasive procedure, such as angioplasty or coronary artery bypass grafting, for high-risk conditions. If necessary, the invasive procedure should be delayed until the patient's condition has stabilized.

Angina, Unstable↗
PubMed1993

Correction of left ventricular ischemia in blacks with hypertensive heart disease.

Among hypertensive patients, blacks are more likely than whites to have ischemia by electrocardiographic and 201Tl-myocardial stress imaging, possibly due to racial differences in the regulation of coronary blood flow or velocity. This investigation was undertaken to determine whether intensive antihypertensive therapy with two or more drugs can correct or reduce ischemia in black hypertensive patients. Thallium myocardial stress imaging and electrocardiographic and echocardiographic studies were performed on 13 black patients with essential hypertension and ischemic heart disease due to hypertensive heart disease (without significant obstructive epicardial coronary artery disease). The studies were made at baseline and after 4 to 48 months of intensive treatment, with a calcium antagonist and an angiotensin converting enzyme (ACE) inhibitor as the main components of the antihypertensive drug regimen. The majority of the patients with abolition or reversal of myocardial ischemia documented by 201Tl-myocardial imaging also had a significant reduction in left ventricular mass (LVM). However, some patients either did not have LV hypertrophy at baseline or had changes in LVM beyond the precision of the echocardiographic M-mode mass calculations. The finding indicated that factors other than reduction of LVM were involved in the reversal of the ischemia. The most likely factor was a change in the regulation of coronary blood flow. Reduction in LVM and reversal of myocardial ischemia determined either by electrocardiography or by thallium myocardial imaging studies may be considered indicators of the effectiveness of treatment.

Adult↗
PubMed1992

Pericarditis and myocarditis. Which is benign and which isn't?

Pericarditis and myocarditis are inflammatory diseases that are often initiated by common viruses. Pericarditis rarely causes serious long-term disability, whereas myocarditis may lead to chronic congestive cardiomyopathy and permanent disability. The pathogenesis of both is proposed to be bimodal, with an early stage characterized by viral replication and a later stage by infiltration of lymphocytes and necrosis of cells secondary to an autoimmune process. Treatment of pericarditis is usually symptomatic. Myocarditis requires bed rest and conventional therapy for congestive heart failure. Efficacy of immunosuppressive therapy for myocarditis is currently being tested in an international multi-center clinical trial.

Humans↗
PubMed1992

Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia.

Patients with the clinical diagnosis of ischemic heart disease who were found to be free of significant coronary artery atherosclerotic disease (n = 150) underwent coronary vasodilator reserve testing, 2-dimensional echocardiography, and dipyridamole limited-stress thallium testing. After exclusions (predominantly for technically poor coronary artery Doppler signals or suboptimal echocardiography), 100 patients formed the study population. The purpose was to characterize typical cardiac and coronary artery findings in hypertensive patients with severe left ventricular (LV) hypertrophy (n = 15) and to investigate the evidence for myocardial ischemia unrelated to coronary atherosclerosis in early and advanced hypertensive heart disease. Normotensive and hypertensive control groups without LV hypertrophy (n = 12 and 34, respectively) were used for comparison. Severe LV hypertrophy was defined as LV mass index greater than or equal to 50% above established gender specific norms using 2-dimensional-directed M-mode echocardiography and the cube equation corrected to agree with necropsy estimates of mass. Clinical characteristics more often associated with severe LV hypertrophy were black race (67%), diabetes mellitus (33%), proteinuria (47%) and elevated creatinine (1.5 +/- 0.9 mg/dl). Baseline electrocardiograms and dipyridamole limited-stress thallium scans were highly likely to be abnormal (94 and 73%, respectively). Both eccentric and concentric cardiac hypertrophies were found in the severe group. Ejection fraction was significantly lower (0.51 vs 0.68, p = 0.002) and basal coronary flow velocity higher (12.0 vs 5.0 cm/s, p = 0.0004) among these patients when compared with normotensive control patients. Coronary flow reserve did not differ between control groups but was significantly depressed in patients with severe LV hypertrophy (2.5 vs 3.9, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Pharmacotherapy of unstable angina.

All patients with unstable angina should be admitted to a coronary or an intensive care unit. There should be an attempt to classify the patient according to the proposed Braunwald nomenclature. If the patient has a secondary cause for unstable angina (e.g., tachyarrhythmia, heart failure, fever, thyrotoxicosis, severe hypertension, hypoxia, unusual emotional stress, or anemia), this condition should be treated initially with therapy specific for that etiology. If the patient does not have a secondary etiology, therapy should be initiated with nitrates, preferably intravenous nitroglycerin. Heparin should be concomitantly administered. If the patient cannot receive heparin, aspirin should be initiated. All patients should receive beta-blockers. If the patient cannot take a beta-blocker, a calcium antagonist (probably diltiazem) should be initiated. However, if the patient is refractory to beta-blockers, the dihydropyridine nifedipine should be added. Failure to all pharmacologic interventions necessitates a progressive invasive approach dictated by the potential surgical risk of the patient. Long-term aspirin and beta-blockers should be strongly considered.

Angina, Unstable↗