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Biomedical subjects

R R Miller

Publications and source records attributed to R R Miller.

At least 325 records · Page 18Linked to original sources
PubMed1976

Afterload reduction therapy with nitroprusside in severe aortic regurgitation: improved cardiac performance and reduced regurgitant volume.

To assess the hemodynamic effects of afterload reduction in severe aortic regurgitation, nitroprusside was infused at cardiac catheterization in 12 patients with aortic regurgitation. Cardiac hemodynamics, angiographic variables and regurgitant volumes were quantified during control periods, and nitroprusside was infused to reduce systemic systolic pressure to 110 to 125 mm Hg. The following were reduced by the drug: systolic arterial pressure (from 154 +/- 6.4 to 115 +/- 2.3 mm Hg, P less than 0.001); left ventricular end-diastolic pressure (from 23 +/- 2.2 to 11 +/- 1.0 mm Hg, P less than 0.001); systemic vascular resistance (from 1,782 +/- 133 to 1,148 +/- 94 dynes sec cm-5, P less than 0.001); left ventricular end-diastolic volume (from 242 +/- 25 to 196 +/- 19 ml, P less than 0.001); aortic regurgitant fraction (from 0.53 +/- 0.05 to 0.44 +/- 0.06, P less than 0.01); and aortic regurgitant minute volume (from 5.5 +/- 0.10 to 4.3 +/- 0.09 liters/min, P less than 0.01). Effective cardiac index increased (from 2.49 +/- 0.19 to 3.10 +/- 0.24 liters/min per m2, P less than 0.01), and left ventricular ejection fraction rose (from 0.55 +/- 0.03 to 0.61 +/- 0.03, P less than 0.005). These data indicate that afterload reduction with nitroprusside in severe aortic regurgitation improves cardiac performance, greatly decreases left ventricular preload and reduces aortic regurgitant volume. Thus, nitroprusside therapy has special value in severe aortic regurgitation that is of particular benefit in critical clinical conditions.

Aged↗
PubMed1976

Comparison of the chemical, physical, and survival properties of normal and Z-variant alpha-1-antitrypsins.

A procedure has been developed for the purification of Z-type alpha-1-antitrypsin (alpha-1-AT) which is rapid, gentle, and results in good yields. From 4 units (750 ml) of fresh human plasma, obtained from two individuals possessing the Pizz phenotype, 53 mg of pure Z-type alpha-1-AT was obtained. The preparation was homogeneous by the criteria of polyacrylamide gel electrophoresis, both in the presence and absence of sodium dodecyl sulfate, and by analytical ultracentrifugation. When compared to pure alpha-1-AT from plasma of individuals possessing the normal PiMM phenotype, the two proteins were indistinguishable with respect to amino acid composition, sedimentation coefficient (s20w of 3.33 for both M and Z), molecular weight (51,000 by sodium dodecyl sulfate gel electrophoresis and 47,000 by sedimentation equilibrium for both M and Z), and trypsin-combining ratio (0.91 for Z and 0.99 for M). The only difference which was observed between the variant forms of alpha-1-AT was in the carbohydrate composition. The Z-type alpha1-AT contains between 20 and 25% less carbohydrate than the M-type alpha-1-AT. Specifically, the Z-type alpha-1-AT is deficient in 1 glucosamine residue, 3 neutral sugar residues (1 mannose and 2 galactose), and 2 sialic acid residues. Although the Z-variant is deficient in sialic acid, its survival time in the serum of a rabbit was not significantly different from that of M-type alpha-1-AT.

Amino Acids↗
PubMed1976

Pump dysfunction after myocardial infarction: importance of location, extent and pattern of abnormal left ventricular segmental contraction.

To delineate the relative effects on left ventricular function of the site, extent and nature of the abnormal left ventricular segmental contraction (dyssynergy) and thereby determine the mechanism by which anterior myocardial infarction results in greater depression of left ventricular performance than does inferior infarction, 43 patients with remote myocardial infarction of similar extent (average 38 percent of left ventricular systolic perimeter) and associated hypokinesia or dyskinesia confined to either the anterior or inferior wall were compared; 10 additional patients were evaluated who exhibited generalized dyssynergy (72 percent of left ventricular perimeter). When the pattern of dyssynergy and extent of infarction were similar, the location alone of dyssynergy did not influence variables of left ventricular function. However paradoxical outward systolic movement (dyskinesia) of the anterior or inferior wall resulted in greater depression (P less than 0.05) of measures of left ventricular performance than did diminished inward systolic motion (hypokinesia) associated with infarction of similar extent and location. All measures of left ventricular performance were considerably more depressed (P less than 0.05) in the 10 patients with generalized dyssynergy than in the 43 patients with localized dyssynergy. Thus, the location of infarction is not a unique determinant of left ventricular performance. Instead, the size of infarction is the principal characteristic of dyssynergy that impairs left ventricular function; the severity of the pattern of dyssynergy is significant but of lesser importance. It is therefore concluded that the greater reduction of left ventricular function in anterior than in inferior myocardial is largely the result of the more extensive area of necrosis rather than of the location of the infarction.

Adult↗
PubMed1976

Functional significance of coronary collateral vessels in patients with acute myocardial infarction: relation to pump performance, cardiogenic shock and survival.

In 20 patients with acute myocardial infarction requiring emergency left heart catheterization and coronary arteriography, ventricular function and clinical course were related to collateral vessels supplying the infarcted area. The major coronary artery to the infarcted region was severely obstructed in all patients. Patients with adequate collateral vessels (Group I, no. = 6) and those with no or inadequate collateral channels (Group II, no. = 14) had similar findings with respect to age, site of infarction, prevalence of prior infarction and presence of multivessel disease. However, there were significant differences between Groups I and II in left ventricular end-diastolic pressure (13 versus 30 mm Hg), cardiac index (3.05 versus 2.04 liters/min per m2), stroke work index (45 versus 13 g-m/m2), ejection fraction (42 versus 20 percent) and area of dyssynergy (14 versus 47 percent). Moreover, in Group I all patients survived and none had cardiogenic shock, whereas in Group II 10 of 14 patients had shock and 8 of 14 died. The rapidity of vessel obstruction appeared to influence collateralization since infarction was preceded by angina pectoris more frequently in Group I than in Group II. These results indicate that well functioning anastomotic channels to the distal trunk of the blocked coronary artery may afford some protection of pump function and improve the prognosis in acute myocardial infarction.

Acute Disease↗
PubMed1976

Mitral valve early diastolic closing velocity in the echocardiogram: relation to sequential diastolic flow and ventricular compliance.

Uncertainty exists regarding the determinants of mitral valve early diastolic closing velocity (E-F slope) in the echocardiogram. Accordingly, the mitral E-F slope, sequential atrioventricular flow in each third of diastole in the cineangiogram and an index of ventricular compliance (delta volume/delta pressure normalized by end-diastolic volume) were obtained in 10 normal subjects, 10 patients with coronary artery disease and marked dyssynergy and 9 patients with hypertrophic cardiomyopathy. The E-F slope of 103 +/- 20 mm/sec (mean +/- standard deviation) in normal subjects was greatly reduced in patients with coronary artery disease and hypertrophic cardiomyopathy (54 +/- 22 and 27 +/- 16 mm/sec, respectively, P less than 0.001). Transmitral flow of 52 +/- 25 cc during the initial third of diastole in normal subjects represented 48 +/- 10 percent of total flow and was diminished in patients with coronary artery disease and hypertrophic cardiomyopathy: 23 +/- 16 cc (25 +/- 24 percent) and 24 +/- 20 cc (20 +/- 11 percent), respectively (both P less than 0.001). The ventricular compliance index in normal subjects of 0.064 +/- 0.02 was also decreased identically in patients with coronary artery disease and hypertrophic cardiomyopathy: 0.029 (both P less than 0.001). The E-F slope was correlated with transmitral flow during the first third of diastole (r = 0.87) but was decreased to a slightly greater extent for any given reduction in flow in patients with hypertrophic cardiomyopathy than in patients with coronary artery disease. Although the E-F slope could not be related to compliance in individual patients, patients with an E-F slope of less than 75 mm/sec nearly always had diminished compliance. Thus, mitral E-F slope is primarily related to transmitral flow in the initial third of diastole. Reduced ventricular diastolic compliance usually results in diminished flow, and thus a decreased E-F slope, in patients with coronary artery disease or hypertrophic cardiomyopathy. The greater reduction in E-F slope for any decrement of flow in hypertrophic cardiomyopathy than in coronary disease may be due either to interference with vortex streaming or to alterations in the relation of the papillary muscles to the mitral valve induced by altered ventricular geometry; the finding indicates that factors in addition to flow may influence the E-F slope.

Adult↗
PubMed1976

Reduction of S-T segment elevation with infusion of nitroprusside in patients with acute myocardial infarction.

The effect of infusion of sodium nitroprusside on S-T segment elevation was evaluated in 12 patients with acute anterior myocardial infarction. Precordial 35 lead S-T segment maps were obtained in each patient immediately before and 10 minutes after infusion of 53 mug/min (range 20 to 100 mug/min) of nitroprusside. The following measurements were made from each S-T map: sigmaST (total S-T elevation in all leads), NST (number of leads with S-T elevation greater than 1 mm) and ST (average (S-T elevation in leads with more than 1 mm elevation). After administration of mitroprusside, evidence of myocardial ischemic injury as assessed by S-T mapping decreased in association with reduction of the myocardial oxygen consumption index of pressure-time per minute. Group mean values diminished significantly for sigmaST (41.7 to 28.6 mm, P less than 0.001), NST (20.3 to 14.6, P less than 0.001) and ST (1.6 to 1.2 mm, P less than 0.005). Pressure-time per minute decreased from 2,690 to 2,372 mm Hg-sec/min (P less than 0.001). Because there was no significant relation (P less than 0.05) between reductions in S-T elevation and lower indexes of myocardial oxygen consumption, it is suggested that nitroprusside may possess a separate action of augmenting regional blood flow to ischemic myocardium. Evaluation with the precordial S-T mapping technique suggested that intravenous administration of nitroprusside was associated with evidence of reduced ventricular ischemic injury in patients with acute myocardial infarction. This effect appears to be related to reduction of myocardial oxygen demand by the peripheral cardiac unloading mechanisms of nitroprusside as well as to a possible direct action of the drug in improving regional blood flow to ischemic heart muscle.

Acute Disease↗
PubMed1976

Myocardial performance and N2O analgesia in coronary-artery disease.

Inhalation of 40 per cent N2O by nine patients who had occlusive disease in two or more coronary arteries with elevation of left ventricular end-diastolic pressures (LVEDP) significantly decreased arterial pressure (average 5 per cent) and myocardial contractility as measured by dP/dt/CPIP (average 14 per cent), and increased LVEDP (average 21 per cent). N2O had no significant effect in four patients who had angina without angiographically demonstrable coronary arterial disease. It is concluded that N2O depresses myocardial function in patients who have occlusion of the coronary arteries and impaired left ventricular function.

Adult↗
PubMed1976

Reduction of ischemic injury by sublingual nitroglycerin in patients with acute myocardial infarction.

The effect of sublingual nitroglycerin (NTG) on myocardial ischemic injury was evaluated in eleven patients with acute anterior myocardial infarction. Precordial 35-lead ST-segment maps were obtained in each patient immediately before and 3-10 minutes after 0.4 mg sublingual NTG. The following measurements were made from each ST map: N-ST (number of leads showing ST elevation greater than 1mm), sigmaST (total ST elevation in all leads), ST (average ST-segment elevation in those leads with less than 1mm elevation). Following 0.4 mg sublingual NTG evidence of myocardial ischemic injury as assessed by ST-segment mapping decreased in association with reduction of heart rate X systolic blood pressure product (10.80 X 10(3) to 9.49 X 10(3), P less than 0.001). Group mean values diminished significantly for N-ST (18.1 to 14.4, P less than 0.001), sigma ST (37.9 to 30.1 P less than 0.005) and ST (1.7 to 1.4, P less than 0.001). Evaluation performed by the technique of precordial ST-segment mapping suggests that sublingual nitroglycerin in a commonly employed clinical dose is associated with evidence of reduced ischemic cardiac injury in patients with acute myocardial infarction. This effect appears to be related to reduction of myocardial oxygen demand by the nitrate.

Acute Disease↗
PubMed1976

Pharmacological mechanisms for left ventricular unloading in clinical congestive heart failure. Differential effects of nitroprusside, phentolamine, and nitroglycerin on cardiac function and peripheral circulation.

We compared cardiocirculatory actions of the commonly employed systemic vasodilators, intravenous (iv) nitroprusside (NP), iv phentolamine (PH), and sublingual nitroglycerin (NTG), causing left ventricular (LV) unloading in 29 chronic coronary subjects with congestive failure to determine whether they produce disparate responses in LV function by different relaxing actions on systemic resistance and capacitance beds. Each drug equally lowered systemic arterial pressures to a small extent, whereas heart rate rose slightly with NTG. Cardiac catheterization showed a decline in end-diastolic pressure with NTG (19 to 8 mm Hg) which was greater (P less than 0.05) than with NP and PH (21 to 11). Cardiac index increased (P less than 0.05) during NP (2.68 to 2.93 liters/min per m2) and PH (2.60 to 3.02) but was unchanged (2.83) by NTG. Stroke work increased with PH, ejection fraction rose with NP and PH, and mean ejection rate increased with each, whereas pressure-time per minute fell and end-diastolic volume decreased with each agent. Total systemic vascular resistance declined (P less than 0.001) during NP and PH (1,475 to 1,200 dynes sec cm-5) but was unchanged (1,487) by NTG. Plethysmographically, forearm vascular resistance (FVR) decreased (P less than 0.01) with NP and PH (61.6 to 39.1 mm Hg/ml per 100 g/min) but not (52.4) by NTG. The decreases in venous tone (VT) with NTG (18.2 to 9.3 mm Hg/ml) and NP (18.5 to 9.8) were greater (P less than 0.05) than with PH (18.8 to 13.1) FVR/VT percent changes of 0.96, 1.62, and 0.53 with NP, PH, and NTG indicated balanced systemic arteriolovenous relaxation by iv NP, greater arteriolar dilation with iv PH, and predominant venous dilation by sublingual NTG. Thus, vasodilators produce disparate modifications of LV function by their differing alterations of preload and impedance, which are dependent upon relative extents of relaxation of systemic resistance and capacitance vessels characteristic of each agent as used clinically.

Adult↗
PubMed1976

Intraventricular free wall dissection causing acute interventricular communication with intact septum in myocardial infarction.

This report delineates a previously unrecognized complication of acute myocardial infarction, an intraventricular wall dissection producing interventricular communication without septal perforation. The clinical, hemodynamic, and pathologic features of this unique condition are documented, as well as the factors important in the mechanism of its production.

Aged↗
PubMed1976

Prevention of lower extremity venous thrombosis by early mobilization. Confirmation in patients with acute myocardial infarction by 125I-fibrinogen uptake and venography.

To determine the effects of early ambulation on peripheral venous thrombosis in the coronary care unit, 29 patients with acute myocardial infarction had daily 125I-fibrinogen point counting of both legs using a standard portable technique in the first 3 to 7 days after admission. Twenty-one patients underwent early ambulation during the initial 3 days, while 8 remained at complete bed rest for 5 days. Only 2 of 21 early ambulated patients had positive fibrinogen point counts, in contrast to 5 of 8 nonambulated patients (P less than 0.01). With heart failure, only 2 of 9 ambulated patients had positive point counts, compared with 4 of 5 nonambulated patients (P less than 0.05). In 16 patients undergoing venography, point counts were confirmed in 6 positive and 10 negative findings. These results show that the high frequency of peripheral venous thrombosis in immobilized acute myocardial infarction patients, particularly those with heart failure, can be effectively reduced by early ambulation.

Acute Disease↗
PubMed1975

Propranolol-withdrawal rebound phenomenon. Exacerbation of coronary events after abrupt cessation of antianginal therapy.

Effects on anginal symptoms of sudden withdrawal of large doses of propranolol or placebo were evaluated in 20 patients in a double-blind crossover efficacy trial requiring sudden cessation of the agent. With propranolol, 160 to 320 mg per day for six and 12 weeks, no patients had increased angina or nitroglycerin use, and there were no hospitalizations or deaths. However, within two weeks of discontinuance of propranolol, untoward ischemic events developed in 10 patients. Six had serious withdrawal complications: intermediate coronary syndrome in three, and ventricular tachycardia, fatal myocardial infarction, and sudden death in one each. In four patients discontinuance of placebo increased anginal symptoms; in the remaining 10, ischemic symptoms were not provoked. The rebound phenomenon was related to degree of pre-propranolol angina and relief of pain by the agent. Thus, chronically administered propranolol should be gradually reduced, and activity restricted during its withdrawal.

Adult↗