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Dive into the research topics where Roy V. Markham is active.

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Featured researches published by Roy V. Markham.


American Journal of Cardiology | 1983

Efficacy of prazosin in the management of chronic congestive heart failure: A 6-month randomized, double-blind, placebo-controlled study

Roy V. Markham; James R. Corbett; Alyce Gilmore; William A. Pettinger; Brian G. Firth

The beneficial effects of acute prazosin therapy in patients with congestive heart failure (CHF) have been well documented; however, its chronic efficacy over several months has not previously been evaluated in a placebo-controlled manner. Therefore, an assessment was made by radionuclide ventriculography of the effect of prazosin, 20 mg/day, on left ventricular ejection fraction and end-systolic and end-diastolic volumes at rest and on peak upright bicycle exercise, as well as its effect on right ventricular ejection fraction at rest, exercise time and work load, and standard clinical variables in 23 patients with stable class III symptoms of CHF. The study consisted of a 6-month randomized, double-blind, controlled evaluation of prazosin versus placebo in patients receiving a stable dose of digitalis and diuretics for at least 1 month. At entry, the prazosin and placebo groups did not differ in any respect. Prazosin caused no demonstrable effect on clinical variables such as status of symptoms, heart rate, mean arterial pressure, and cardiothoracic ratio when compared with placebo. Prazosin also caused no demonstrable effect compared with placebo on absolute or percent changes in radionuclide variables at rest or on peak exercise, or on exercise time or exercise work load. In addition, prazosin had no consistent effect compared with placebo on plasma renin activity or plasma catecholamine levels. However, there was a slight but significant increase in weight (p less than 0.0001) and in plasma renin activity in the upright position (p less than 0.002) with time, as well as a tendency for the diuretic dose to increase with time in both groups. Thus, long-term prazosin therapy generally produces no demonstrable subjective or objective improvement in patients with stable, chronic class III CHF receiving digitalis and diuretic therapy.


American Journal of Cardiology | 1982

Hemodynamic and electrophysiologic effects of verapamil and nifedipine in patients on propranolol

Michael D. Winniford; Roy V. Markham; Brian G. Firth; Pascal Nicod; L.David Hillis

Abstract Because the combined use of a beta-adrenergic blocking agent and a calcium antagonist may be beneficial in patients with severe angina, we assessed the hemodynamic and electrophysiologic effects of verapamil or nifedipine in patients receiving oral propranolol. In 26 patients with stable angina receiving oral propranolol (234 ± 230 mg/day, mean ± standard deviation), cardiac catheterization was performed, and variables were measured at baseline and 5 to 10 minutes after (1) intravenous saline solution, 10 ml (n = 6); (2) intravenous verapamil, 0.15 mg/kg body weight to a maximal dose of 10 mg (n = 10); and (3) sublingual nifedipine, 10 mg (n = 10). Cardiac output (by thermodilution) was unchanged after saline solution and verapamil but increased with nifedipine (4.3 ± 1.1 to 5.0 ± 1.4 liters/min, p


American Journal of Cardiology | 1983

Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia

Roy V. Markham; Michael D. Winniford; Brian G. Firth; Pascal Nicod; Gregory J. Dehmer; Samuel E. Lewis; L.David Hillis

Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 +/- 0.11 [mean +/- standard deviation] before pacing to 0.67 +/- 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by greater than 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression greater than or equal to 0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF greater than or equal to 0.05 (0.46 +/- 0.10 to 0.33 +/- 0.09, p less than 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of greater than 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.


American Journal of Cardiology | 1982

Assessment of Vasodilator Therapy in Patients With Severe Congestive Heart Failure: Limitations of Measurements of Left Ventricular Ejection Fraction and Volumes

Brian G. Firth; Gregory J. Dehmer; Roy V. Markham; James T. Willerson; L.David Hillis

Although noninvasive techniques are often used to assess the effect of vasodilator therapy in patients with congestive heart failure, it is unknown whether changes in noninvasively determined left ventricular ejection fraction, volume, or dimension reliably reflect alterations in intracardiac pressure and flow. Accordingly, we compared the acute effect of sodium nitroprusside on left ventricular volume and ejection fraction (determined scintigraphically) with its effect on intracardiac pressure and forward cardiac index (determined by thermodilution) in 12 patients with severe, chronic congestive heart failure and a markedly dilated left ventricle. Nitroprusside (infused at 1.3 +/- 1.1 [mean +/- standard deviation] microgram/kg/min) caused a decrease in mean systemic arterial, mean pulmonary arterial, and mean pulmonary capillary wedge pressure as well as a concomitant increase in forward cardiac index. Simultaneously, left ventricular end-diastolic and end-systolic volume indexes decreased, but the scintigraphically determined cardiac index did not change significantly. Left ventricular ejection fraction averaged 0.19 +/- 0.05 before nitroprusside administration and increased by less than 0.05 units in response to nitroprusside in 11 of 12 patients. The only significant correlation between scintigraphically and invasively determined variables was that between the percent change in end-diastolic volume index and the percent change in pulmonary capillary wedge pressure (r = 0.68, p = 0.01). Although nitroprusside produced changes in scintigraphically determined left ventricular ejection fraction, end-systolic volume index, and cardiac index, these alterations bore no predictable relation to changes in intracardiac pressure, forward cardiac index, or vascular resistance. Furthermore, nitroprusside produced a considerably greater percent change in the invasively measured variables than in the scintigraphically determined ones.


American Journal of Cardiology | 1983

Central and regional hemodynamic effects and neurohumoral consequences of minoxidil in severe congestive heart failure and comparison to hydralazine and nitroprusside

Roy V. Markham; Alyce Gilmore; William A. Pettinger; D. Craig Brater; James R. Corbett; Brian G. Firth

Minoxidil is a potent oral vasodilator of potential value in patients with congestive heart failure (CHF), although preliminary studies show that it causes fluid retention. To test whether minoxidil acts primarily as an arterial vasodilator in CHF, it was compared with hydralazine and nitroprusside. To evaluate its chronic efficacy and mechanism of fluid retention, the effects of minoxidil (7 patients) were compared, in a double-blind manner, with those of hydralazine (8 patients) on central and regional hemodynamics and the renin-angiotensin-aldosterone and sympathetic nervous systems. There was no demonstrable difference in the central hemodynamic effects of minoxidil and hydralazine in the dosages used. After 6 hours both drugs increased cardiac index (minoxidil group, from 1.65 ± 0.29 to 2.26 ± 0.40 liters /min/m2, p < 0.0001; hydralazine group, from 1.88 ± 0.61 to 2.34 ± 0.90 liters/min/m2, p < 0.0001), decreased systemic vascular resistance and increased heart rate without change in pulmonary arterial, pulmonary capillary wedge or right atrial pressures. Nitroprusside effects differed from those of minoxidil and hydralazine with respect to heart rate (p < 0.005) and mean pulmonary arterial (p < 0.007) and right atrial (p < 0.009) pressures. Nitroprusside also decreased relative hepatomesenteric flow compared with the other 2 agents (p < 0.005). Neither renal blood flow, glomerular filtration rate, filtration fraction, nor urinary sodium excretion were significantly altered acutely by any of the 3 drugs. Minoxidil and hydralazine did not differ in their neurohumoral effects: Both agents produced an increase in plasma norepinephrine concentration (p < 0.003) and plasma renin activity (p < 0.04), but no change in plasma epinephrine or aldosterone concentrations. After 1 week of double-blind therapy, fluid retention was a greater problem with minoxidil than with hydralazine. Thus, minoxidil behaves primarily as an arterial vasodilator in CHF, fluid retention is a severe adverse effect, and the greater degree of fluid retention with minoxidil than hydralazine is not attributable to differing acute effects on total renal blood flow or function, or differing effects on the renin-angiotensin-aldosterone or sympathetic nervous systems.


American Heart Journal | 1981

Evaluation of postextrasystolic T wave alterations in identification of patients with coronary artery disease or left ventricular dysfunction

D.Richard Leachman; Gregory J. Dehmer; Brian G. Firth; Roy V. Markham; Michael D. Winniford; L.David Hillis

This study was performed (1) to assess the value of postextrasystolic T wave alterations in identification of patients with cardiac disease and (2) to determine if their frequency depends on length of compensatory pause. In 52 patients a pacing catheter was placed in the right ventricular (RV) apex, and premature beats were programmed to occur 30 msec beyond RV refractory period. Postextrasystolic T wave alterations occurred in 32 patients, 13 with an 19 without coronary artery disease (CAD) (NS). Such alterations were also not related to presence of abnormal left ventricular (LV) ejection fraction (less than 0.55) or end-diastolic pressure (greater than 12 mm Hg). In 33 patients, premature beats were also introduced 330 msec beyond the RV refractory period to compare effects of long and short compensatory pauses on frequency of postextrasystolic T wave alterations. When the pause was near maximal, 18 patients had alterations in 60 ECG leads; when it was shorter, seven patients had alterations in 10 leads (p less than 0.001). Thus, judging from provoked postextrasystolic T wave alterations, such spontaneous changes appear neither sensitive nor specific in the identification of patients with cardiac disease. The frequency of postextrasystolic T wave changes depends on the length of the compensatory pause.


American Journal of Cardiology | 1980

Effect of selective coronary arteriography on left ventricular volumes and ejection fraction in man

Lawrence Stern; Brian G. Firth; Gregory J. Dehmer; Stacey M. Johnson; Roy V. Markham; Samuel E. Lewis; L. David Hillis

This study was performed to assess the influence of selective coronary arteriography on left ventricular volumes and ejection fraction in man. In 30 patients with assorted cardiac diseases, left ventricular end-diastolic and end-systolic volumes and ejection fraction were quantitated immediately before and after selective coronary arteriography. In 19 patients (Group A), contrast left ventriculography was performed immediately before and after selective coronary arteriography. In the remaining 11 patients (Group B), multigated equilibrium blood pool imaging was performed just before and after coronary arteriography. In both groups, mean systemic arterial pressure and heart rate did not change from just before the first to immediately before the second assessment of left ventricular volumes and ejection fraction, but left ventricular end-diastolic pressure increased. End-diastolic and end-systolic volume indexes, and ejection fraction did not change from just before to immediately after selective coronary arteriography. Therefore, selective coronary arteriography (1) consistently causes an increase in left ventricular end-diastolic pressure but (2) exerts no effect on left ventricular volumes and ejection fraction, even in patients with severely compromised left ventricular function.


The American review of respiratory disease | 2015

Independence of Oxygen Consumption and Systemic Oxygen Transport in Patients with Either Stable Pulmonary Hypertension or Refractory Left Ventricular Failure1–4

Timothy R. Chappell; Lewis J. Rubin; Roy V. Markham; Brian G. Firth


Catheterization and Cardiovascular Diagnosis | 1982

The myocardial oxygen supply/demand ratio in patients with and without coronary artery disease

Gregory J. Dehmer; Michael D. Winniford; L. David Hillis; Roy V. Markham; Brian G. Firth


American Journal of Cardiology | 1982

Determinants of maximal exercise capacity in congestive cardiomyopathy

Roy V. Markham; James R. Corbett; William A. Pettinger; Pascal Nicod; Samuel E. Lewis; Alyce Gilmore; Brian G. Firth

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Brian G. Firth

University of Texas Southwestern Medical Center

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L.David Hillis

Parkland Memorial Hospital

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Michael D. Winniford

University of Mississippi Medical Center

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Alyce Gilmore

University of Texas System

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James R. Corbett

University of Texas System

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L. David Hillis

University of Texas Southwestern Medical Center

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Samuel E. Lewis

University of Texas System

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William A. Pettinger

University of Texas Health Science Center at San Antonio

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