Asunto(s)

Asunto(s)

RESUMEN

Cardiovascular morbidity and mortality remain high in ESRD patients. Lipid abnormalities in CAPD may be more important than in hemodialysis. Vessel calcification may have a role in atherosclerotic heart disease, but this is only an inference from several clinical observations, and it remains to be defined more clearly as a risk factor. Left ventricular hypertrophy is frequent in this patient population, and is associated with specific clinical patterns and an increased risk of death. Erythropoietin treatment of anemia and tight blood pressure controls have proved to help in reversing severe left ventricular hypertrophy. Finally, we describe a syndrome of the hypertrophic, high cardiac output hemodialysis heart, which is characterized by a high cardiac output in hemodialysis patients. It is associated with left ventricular hypertrophy and eventually right ventricular hypertrophy with tricuspid insufficiency. This may require fistula revision and even a switch peritoneal dialysis.

Asunto(s)

RESUMEN

A 53-year-old female presented with disabling chest pain. The pain had most of the characteristics of ischemic pain; however, the results of the initial clinical investigation were consistent with the diagnosis of syndrome X. That is, her treadmill exercise test was positive but her coronary angiogram was normal. A dipyridamole-thallium test resulted in severe chest pain, marked ST abnormalities, but no evidence of any focal reduction in flow. A dipyridamole stress echocardiogram revealed that left ventricular function was entirely normal during the dipyridamole-induced pain and ST segment abnormalities, making ischemia an unlikely cause for either. To attempt to account for this paradox, the hypothesis was generated that both the pain and ST segment abnormalities were due to a primary abnormality of adenosine metabolism rather than secondary to ischemia. Accordingly, adenosine-MIBI scans were done with and without pretreatment with aminophylline. Infusion of adenosine virtually immediately resulted in crushing chest pain and profound ST abnormalities again without any evidence of focal abnormalities of MIBI estimated flow. By contrast, administration of adenosine after pretreatment with aminophylline failed to produce either chest pain or ST abnormalities. Moreover, long term therapy with aminophylline almost entirely relieved the symptoms which had been so distressing. This case indicates that there is a subset of patients with syndrome X--in which faults in adenosine metabolism result in excessive adenosine accumulation or effect and this results, in turn, in adenosine-induced ischemic-like chest pain and adenosine-induced ST abnormalities. There is, however, no actual ischemia of the myocardium. Given the known effects of adenosine on coronary flow, the problem in this subset of patients appears to be equivalent to an attack of myocardial migraine and blockers of adenosine action might be of help to other patients with a similar pathophysiology for their chest pain.

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

A 67-year-old female presented seven years after insertion of a mitral prosthesis with mild to moderate pulmonary edema and severe right heart failure with pulmonary and tricuspid insufficiency. Clinical examination and noninvasive tests did not demonstrate prosthetic valve dysfunction. Cardiac catheterization revealed a marked V wave but no mitral regurgitation and no significant mitral diastolic gradient. A clinical diagnosis of a stiff left atrium was made and confirmed at autopsy. The pathophysiology of the syndrome is discussed.

Asunto(s)

RESUMEN

Reflected pressure waves returning to the ascending aorta are an important contribution to aortic systolic pressure and thus the load on the left ventricle. The effect of glyceryl trinitrate on pressure wave reflections in the ascending aorta was studied using the transmission of arterial pressure between two high fidelity pressure transducers. Glyceryl trinitrate 0.3 mg sublingually reduced systolic arterial pressure by 11 mmHg owing to a reduction of the late systolic pressure peak. Mean arterial pressure fell 2 mmHg, but heart rate and aortic flow did not change. The aortic input impedance was reduced at the first harmonic (control 18.4(4.1); glyceryl trinitrate 10.8(2.4) kPa.s.litre-1; p less than 0.005) but characteristic impedance was not changed (control 12.7(3.8); glyceryl trinitrate 14.2(3.3) kPa.s.litre-1). The first two harmonics of apparent phase velocity were reduced by glyceryl trinitrate (1.05 Hz: control 3314(798); glyceryl trinitrate 1772(495) cm.s-1; p less than 0.01; 2.1 Hz: control 1246(269); glyceryl trinitrate 754(127) cm.s-1; p less than 0.05), yet the foot to foot wave velocity was unchanged (control 688(112); glyceryl trinitrate 726(112) cm.s-1). There was a significant reduction in the amplitude of the global reflection coefficient at 1.05 Hz (control 0.70(0.09); glyceryl trinitrate 0.48(0.08); p less than 0.001) and at 2.1 Hz (control 0.48(0.07); glyceryl trinitrate 0.23(0.06); p less than 0.005) with no significant change in phase. Glyceryl trinitrate reduces cardiac pulsatile load by diminishing the amplitude of wave reflections arriving back in the aorta during systole yet has no effect on aortic compliance or arteriolar resistance. This study demonstrates a method of evaluating the effect of vasoactive drugs on cardiac pulsatile load.

Asunto(s)

RESUMEN

It has previously been shown that nitroglycerin increases the compliance of forearm arteries. The present study investigates whether nitroglycerin reduces the hydraulic load on the heart (as measured by aortic input impedance) by a mechanism compatible with an increase in peripheral arterial compliance. In eight subjects, measurements of aortic flow and pressure were made with a catheter tipped probe before and during intravenous nitroglycerin (6 to 30 micrograms/min) administration. The reduction of aortic systolic pressure (129 +/- 5 to 113 +/- 4 mmHg, P less than 0.001) was due to a decrease in the late systolic pressure peak. There was no change in stroke volume, heart rate or systemic vascular resistance. The lower systolic pressure resulted from a decrease in the amplitude of the first harmonic of input impedance (210 +/- 19 to 143 +/- 11 dyne.s.cm-5, P less than 0.005) yet characteristic impedance (a measure of local aortic distensibility) did not change. The ratio of maxima to minima of the impedance spectrum was reduced (1.02 +/- 0.09 to 0.71 +/- 0.11, P less than 0.05) suggesting a decrease in the amplitude of reflected waves contributing to aortic impedance. Nitroglycerin at doses which have no effect on arteriolar resistance vessels, reduces systolic aortic pressure by diminishing the amplitude of wave reflections returning to the ascending aorta in late systole. This mechanism is compatible with the peripheral arterial effects of nitroglycerin.

Asunto(s)

RESUMEN

Twenty-four patients referred for cardiac catheterization for suspected aortic stenosis were investigated by equilibrium gated blood pool study. From the time-activity curves, end systole for each ventricle was determined and the delay between the two was calculated. The patients were divided into three groups according to their calculated aortic valve area. The mean delay in a control group of 20 normal subjects was 6 +/- 13 msec (mean +/- standard deviation). In group I (aortic valve area greater than 0.75 cm2) the delay was 16 +/- 25 msec (p = NS compared to controls); in group II (aortic valve area 0.5 to 0.75 cm2) the delay was 28 +/- 27 msec (p less than 0.01); and in group III (aortic valve area less than 0.5 cm2) the delay was 60 +/- 28 msec (p less than 0.001). Ten patients were restudied after valve replacement; their mean delay decreased markedly from 48 +/- 19 to 5 +/- 26 msec (p less than 0.001). Thus, this method appears to identify patients with severe aortic stenosis and may therefore be a useful adjunct to the noninvasive assessment of this disorder both before and after surgery.

Asunto(s)

RESUMEN

This report tests the hypothesis that, in early diastole, motion of the anterior left atrial wall corresponds to the motion that can be observed in the contiguous posterior wall of the aortic root. To test this hypothesis, we examined the effects of mitral stenosis, exercise in normals, exercise induced left ventricular ischemia, left ventricular hypertrophy and left ventricular dysfunction on this slope. Each altered early diastolic atrioventricular interaction as predicted and therefore, the early diastolic motion of the anterior left atrial wall does appear to be mirrored by the early diastolic slope of the posterior wall of the aortic root. Consequently, if interpreted in the clinical context, measurement of early diastolic slope of the posterior wall of the aortic root may serve as a useful guide to separate patients with severe from those with mild mitral stenosis.

Asunto(s)

RESUMEN

Recent studies indicate that predischarge evaluation of the post-myocardial infarction (MI) patient is important in predicting their subsequent course and the need for specific treatment. Left ventricular function, residual ischemia and the tendency toward ventricular arrhythmias can all be assessed noninvasively in the late hospital phase. Stress testing is 1 of the most useful and widely available of these techniques. An impaired hemodynamic response to exercise expressed by excessive tachycardia, plateau or falling blood pressure or reduced work load capacity suggests an increased risk of recurrent cardiac events in the near future. Angina or electrocardiographic abnormalities, including arrhythmias, also indicate a less favorable outcome. A good performance in a post-MI stress test is associated with a relatively good prognosis. The exercise electrocardiogram, therefore, appears to be a useful screening device for evaluating post-MI patients. Other noninvasive tests such as radionuclide ventriculography, exercise thallium scanning, Holter monitoring and echocardiography greatly augment the predictive value of exercise electrocardiography, and a patient profile should be developed using all the available clinical and laboratory data. Patients with a poor prognostic profile may then undergo further testing, such as coronary angiography, and their subsequent therapy modified appropriately.

Asunto(s)

RESUMEN

We studied the clinical outcomes of 46 patients followed prospectively for the initial 6 months after inferior infarction. Twenty-one patients (Group A) had no anterior ST depression (V2 to V4) present during the acute phase of the inferior infarction, whereas 25 patients (Group B) had such findings transiently. Although the clinical course during hospitalization was similar in the two groups, that after discharge differed. Only one of 21 patients in Group A had exertional angina and none had rest angina during follow-up; no infarcts or deaths occurred. In contrast, 15 patients in Group B had exertional angina; 12 also had rest pain (p less than 0.001, exact probability test). Two patients had reinfarction, one of whom died, and one sudden death also occurred. Of 15 patients in Group B who had cardiac catheterization, only eight had significant lesions in the anterior vessels, whereas seven did not; six of the seven patients became asymptomatic during follow-up without surgical therapy. Thus, electrocardiograms taken during the early phases of inferior myocardial infarction may be a valuable tool to recognize patients likely to have further ischemic symptoms during the early follow-up period.

Asunto(s)

RESUMEN

A case of ventricular false aneurysm withe the typical clinical, radiological, electrocardiographic, and angiographic features of this entity is presented. The distinction between false ventricular aneurysm and true aneurysm is discussed. This distinction is important because of the propensity of false aneurysms to rupture. An early diastolic murmur was present prior to, but not after, resection of the aneurysmal sac. A theory as to the origin of this murmur is offered.

Asunto(s)

RESUMEN

Most patients with coronary artery disease do not have elevated plasma or low density lipoprotein (LDL) cholesterol. To test whether the protein moiety of LDL, LDL B, might be a parameter to identify ischemic heart disease, the plasma cholesterol, triglyceride, LDL cholesterol, and LDL B were measured in 100 consecutive patients undergoing cardiac catheterization. On the basis of coronary angiography, these patients were divided into two groups: group I, 31 patients without, and group II, 59 patients with significant coronary artery disease. Although cholesterol, triglyceride, and LDL cholesterol levels were all significantly higher in group II, discriminant analysis indicated that LDL B concentrations most clearly separated the two groups. In group I (noncoronary), LDL B was 82 +/- 22 mg/100 ml, whereas in group II, LDL B was 118 +/- 22 mg/100 ml. The B protein level in group I was similar to other normal groups studied (35 asymptomatic male physicians, 83 +/- 11 mg/100 ml; 90 normolipidemic medical students, 72 +/- 17 mg/100 ml). The results therefore indicate that not only does LDL B better separate coronary and noncoronary groups than other lipid parameters studied, but also, among those with coronary artery disease, there exists a group with normal LDL cholesterol but with levels of LDL B protein similar to those observed in type II hyperlipoproteinemia. The explanation for the altered LDL composition observed in this group remains to be elucidated.

Asunto(s)

Asunto(s)

RESUMEN

The motion of the posterior wall of the normal left atrium has not been studied systematically. The superoposterior portion of the left atrium is adynamic throughout the cardiac cycle, whereas the inferoposterior portion is displaced posteriorly with left atrial filling during ventricular systole. In the present study, the left atrial diameter (LAD), the left atrial systolic motion (LASM) and the left atrial systolic velocity (LASV), were determined in the following groups of patients: 34 normals; eight patients with either coronary artery disease or aortic stenosis; six patients with aortic insufficiency; and three patients with ventricular septal defect. The results obtained were compared to 15 patients with angiographically documented mitral regurgitation. In the last group, the LAD (4.2 +/- .19 cm) and LASV (12.3 +/- 1.23 cm) and LASM (1.2 +/- 0.4 cm) were significantly greater reflecting the early accentuated filling of the left atrium induced by mitral regurgitation. As well, the product of these three parameters was greater in the mitral regurgitation group (63.2 +/- 7.34 cm3/sec) than in the other groups and patients with mild to moderate regurgitation had a significantly lower value than those with moderate to severe regurgitation (45.7 +/- 4.1 vs 78.5 +/- 10.9, P less than 0.02). The left atrial echocardiogram, therefore, is an aid in the diagnosis of mitral regurgitation and provides a rough index of the severity of the lesion.

Asunto(s)

RESUMEN

The mechanism(s) by which cholesterol returns to the splanchnic bed from peripheral tissues are not well understood. To study this phenomenon in fasting man, lipoproteins were isolated from plasma obtained from hepatic vein and aorta. Cholesterol content of each lipoprotein class was determined and arteriovenous (AV) differences could be calculated for each patient. The results in the first 24 patients indicated splanchnic secretion of very low density lipoprotein cholesterol (mean AV difference - 3 mg/100 ml, P < 0.01), but not significant AV difference for total cholesterol, high density lipoprotein cholesterol, or low density lipoprotein (LDL) B protein. In contrast, for LDL (d 1.006-1.063 g/ml), there was significant uptake of cholesterol across the AV bed +8 mg/100 ml, P < 0.0002). In a further 15 patients, similar samples were obtained and intermediate density lipoprotein isolated at d 1.006-1.019 g/ml and LDL at 1.019-1.063 g/ml. The AV difference previously noted could now be localized to the 1.019-1.063 cholesterol ester moiety (+8 mg/100 ml, P < 0.0005). In the final 14 patients, the LDL cholesterol AV difference was again confirmed and shown to be unrelated to heparin. As well, there was secretion of triglyceride in the hepatic vein LDL. These quantitative data obtained in man raise the possibility that LDL rather than high density lipoprotein transports cholesterol ester to the splanchnic bed.

Asunto(s)

RESUMEN

To elucidate the mechanism by which left ventricular and diastolic pressure (LVEDP) is reduced by practolol, ventricular volumes, hemodynamics, and diastolic elastic stiffness were determined before and 10 min after intravenous practolol (400 mug/kg) in 12 patients. Heart rate decreased in all patients after practolol (avg., --9/min, p less than 0.02). There was an insignificant increase in stroke work index and decrease in cardiac index attributable to the fall in rate. Practolol did not change and diastolic volume or ejection fraction, but the average LVEDP fell from 21 to 15 mm Hg (p less than 0.01) which was sustained even with atrial pacing to prepractolol heart rates. Diastolic elastic stiffness was also reduced after practolol (0.665 to 0.593, p less than 0.0025). The data indicate that practolol exerts a negative chronotropic effect on the intact heart and, in contrast to other beta blockers such as propranolol, appears to decrease diastolic stiffness in the left ventricle.

Asunto(s)

RESUMEN

The contrast agents used for cardiac angiography have pharmacologic effects on the myocardium and on peripheral and coronary circulations. These effects are a stress to the left ventricle. We have studied the sequential changes in heart rate, LVEDP, positive and negative dP/dt in 34 patients following left ventriculography. These patients were divided into three groups: nine normal patients, 14 patients with valvular or coronary artery disease and abnormal left ventricular function at rest, and 11 patients with significant coronary artery stenosis but normal left ventricular function at rest. Changes in dP/dt most clearly defined the normal and abnormal response. In the normal group the mean positive dP/dt rose abruptly at 30 sec after the ventriculogram, whereas the abnormal group showed a mean decrease. The extent of change varied, however, for patients within each group. Negative dP/dt decreased in both groups but more so in the abnormal group. As did the other groups, patients with coronary artery disease but with normal ventricular function showed individual variation in response. Their mean changes in positive and negative dP/dt were intermediate. Positive dP/dt decreased at 30 sec (similar to, but less than, the group with abnormal ventricular function) and negative dP/dt also diminished at 30 sec with a mean value between the normal and abnormal groups. The results of this study support the concept that left ventricular dysfunction may be elicited by the stress of contrast injection. More importantly, such dysfunction seen both with abnormal and normal left ventricles at rest, may be reflected by the relatively simple measurement of positive dP/dt after ventriculography.

Asunto(s)