Diagnostic and therapeutic implications: exploration through case discussions.
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Biomedical subjects
Publications and source records attributed to J Ferlinz.
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A double-blind randomized study was performed to compare the efficacy of intravenous verapamil with saline in 28 patients with a rapid ventricular rate and atrial fibrillation or atrial flutter. Conversion of atrial fibrillation to sinus rhythm occurred in none of 14 patients after saline and in 3 of 20 patients (15%) 7 to 160 min after verapamil. The ventricular rate in atrial fibrillation was slowed greater than or equal to 15% in 2 of 14 patients (14%) by saline, in 17 of 20 patients (85%) by 1 dose of verapamil (p less than 0.001), and in 19 of 20 patients (95%) by 1 or 2 doses of verapamil (p less than 0.001). Conversion of atrial flutter to sinus rhythm occurred in none of 4 patients after saline and in 1 of 7 patients (14%) 105 min after verapamil. The ventricular rate in atrial flutter was slowed greater than or equal to 15% in none of 4 patients by saline, in 4 of 7 patients (57%) by 1 dose of verapamil, and in 7 of 7 patients (100%) by 1 or 2 doses of verapamil (p less than 0.001).
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Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.
In order to evaluate the effects of rapid digitalization on LV volumes, ejection fraction, and asynergy, 21 patients without heart failure were studied with a combination of hemodynamic and angiographic techniques before and after administration of intravenous ouabain (0.007 mg./Kg.). Seven patients had no CAD and served as normal (control) subjects (Group I), while 14 patients had extensive coronary disease (Group II). All pre-ouabain parameters were within the normal limits in Group I. After ouabain infusion, all indices of LV contractility: dP/dt, VCF, and ejection fraction rose significantly in the normal group, while LV filling pressure and end-diastolic volume remained unchanged. The baseline hemodynamic and volumetric values for Group II patients corresponded closely to their normal (Group I) counterparts, and exhibited similar changes after ouabain administration. Eight patients in Group II also had regional disorders of LV contractility, delineated by 23 abnormal hemiaxes of shortening. After ouabain, 15 out of 23 asynergic segments (65 per cent) improved, seven remained unchanged, and one worsened. It is therefore concluded that rapid digitalization not only enhances LV performance in normal subjects and in patients with CAD, but can also markedly reduce the extent of LV asynergy.
We evaluated the effect of breathing 100 ppm of carbon monoxide versus compressed, purified air for 1 hour on exercise performance in 10 patients with chronic obstructive pulmonary disease in a double-blind, randomized, crossover study. The mean arterial carboxyhemoglobin was 1.48 per cent in the carbon monoxide control period and increased from 1.43 to 4.08 per cent after breathing carbon monoxide (P less than 0.001). The mean arterial carboxyhemoglobin level was 1.52 percent in the air control period and decreased from 1.47 to 1.34 per cent after purified air (P less than 0.001). The mean exercise time until marked dyspnea decreased from 218.5 seconds in the carbon monoxide control period to 146.6 seconds after breathing carbon monoxide (P less than 0.001). The mean exercise time was 219.9 seconds in the air control period and 221.3 seconds after purified air (P not significant). Breathing 100 ppm of carbon monoxide for 1 hour caused a significant reduction in exercise performance in patients with chronic obstructive pulmonary disease.
An area-length expression for RV volume determination from single plane cineangiograms has been developed and verified against the biplane volumes with the aid of the RV human casts. A close correlation was found to exist between the two methods (r = 0.93). Ten patients with normal hearts were subsequently studied. Biplane and single plane RV cineangiogrpahic analyses yielded virtually identical results. The single plane expression was equally valid in the end-systolic and the end-diastolic volume analysis.
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The effects of coronary artery disease on patterns of left ventricular contractility have been thoroughly investigated. In contrast, little is known about the incidence of right ventricular dysfunction induced by this disease. To evaluate the frequency of right ventricular asynergy, biplane right ventricular cineangiograms were obtained in 26 patients. Seven segmental axes of shortening were analyzed in each end-systolic and end-diastolic frame and normalized as percent decrease (or increase) in axis from end-diastolic length. Of 26 patients, 8 (Group I) served as normal (control) subjects. The remaining 18 patients had significant coronary artery disease; 6 of these (Group II) had no significant disease of the right coronary artery, whereas 12 (Group III) had significant obstruction of this artery. Four patients in Group II had a previous anteroseptal myocardial infarction, and six in Group III had a previous inferior myocardial infarction. There was a progressive decrease in segmental axes of shortening from Group I to II and from Group II to II, but the decrease was not significant at the level P less than 0.01. Only one patient in Group II had frank dyskinetic segmental motion of the interventricular septum (this patient had had a previous anteroseptal myocardial infarction), whereas two patients in Group III had dyskinetic segmental motion of the free right ventricular wall (both had previous inferior myocardial infarction). Therefore, coronary artery disease seldom produces significant right ventricular asynergy. Abnormal septal motion is associated with previous anteroseptal myocardial infarction; however, dyskinetic motion of the free right ventricular wall occurs only in patients with a right coronary arterial lesion and previous inferior myocardial infarction.
Since the advent of cardiovascular angiography only a few decades ago (1), a massive number of data related to the ventricular function have been accumulated. Specifically, left ventricular (LV) geometry, volumes, and patterns of contractility have been extensively investigated (2-7), especially in patients with coronary artery disease (8-11). In contrast, much less attention has been given to the characteristics of the right ventricle (RV). This has been due partially to the fact that the LV was always considered to be more important chamber of the heart. The relative neglect of RV performance has been further compounded by difficulties in analyzing the geometry of the RV chamber: while the LV configuration approximately resembles an ellipsoid of revolution (and therefore lends itself to relatively simple mathematical analysis), the RV has always been considered a somewhat amorphous structure that does not yield to simple geometric manipulation. In this review, recent approaches to the angiographic measurements of RV volumes and ejection fraction are examined.
In order to compare levophase ("forward") ventriculograms to standard (selective) LV cineangiography, 10 patients with coronary artery disease were studied by (1) selective injection of contrast medium into the LV cavity followed by (2) injection into the right ventricle and filming the levophase. Biplane cineangiograms were used to calculate the end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI), and ejection fraction (EF). Values for the two respective techniques were then compared. Not only were correlation coefficients for the two methods low, but there was also a statistically significant difference between the two SVI (66 +/- 26 ml. for selective and 53 +/- 25 ml. for levophase injection; p less than 0.02) and the two EF (67 +/- 7 per cent for selective and 52 +/- 12 per cent for levophase injection; p less than 0.01). Levophase cineangiograms therefore significantly underestimate the LV ejection fraction when compared to standard (selective) LV cineangiography. These differences must be considered when evaluating greatly divergent interinstitutional survival rates for patients with low EF who undergo coronary artery bypass surgery, and when selecting candidates for bypass surgery on the basis of the angiographic data.
The effect of timolol versus propranolol on hypertension, hemodynamics, and plasms renin activity was evaluated in 20 men. After two weeks of placebo, 11 men received timolol 30 to 60 mg daily, and nine men received propranolol, 240 to 480 mg daily, for five weeks in a double-blind randomized study. The 20 men then received placebo again for two weeks. Right heart catheterization was performed in all 20 patients after two weeks of the first placebo and after five weeks of timolol or propranolol. Equipotent doses of timolol and propranolol were equally effective in significantly lowering supine and upright systolic and diastolic blood pressure and heart rate recorded on an outpatient basis. Equipotent doses of timolol and propranolol caused similar hemodynamic effects including similar significant depression of cardiac index. Equipotent doses of timolol and propranolol caused similar marked depression of plasma renin activity. The hypotensive action of timolol and of propranolol was unrelated to their effect on plasma renin activity.
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While left ventricular (LV) performance in patients with coronary artery disease (CAD) has been extensively investigated, little attention has been given to right ventricular (RV) function in this disease. For this purpose, a new geometric model for RV volume has been developed and RV end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI) and ejection fraction (EF) have been determined from biplane RV cineangiograms in 26 patients. Eight patients served as normal (control) subjects (group I). Eighteen patients with obstructive CAD comprised two other groups: six who had no significant disease of the right coronary artery (RCA) (group II) and 12 who had a high grade RCA lesion (group III). The mean values for EDVI, SVI and EF in group I were 76 +/- 11 ml/m2, 50 +/- 6 ml/m2, and 66 +/- 6%. The only significant difference between groups I and II was that SVI was lower in group II than in group I (P less than 0.01). No measurements in groups II and III were statistically different from each other. However, markedly subnormal values were found in group III (EDVI: 61 +/- 16 ml/m2, SVI: 33 +/- ml/m2 and ef: 52 +/- 7%); all values being significantly lower (SVI and EF: P less than 0.001; EDVI: P less than 0.05) than in group I. RV end-diastolic pressure was normal in all patients. These findings may related to 1) reduced RV compliance, 2) distorted LV geometry, 31 possible RV ischemia or 4) reduced Frank-Starling effect.