Search PubMed⌕ Search

Biomedical subjects

N Reichek

Publications and source records attributed to N Reichek.

At least 109 records · Page 6Linked to original sources

Matching of myocardial oxygen consumption to mechanical load in human left ventricular hypertrophy and dysfunction.

The coupling of myocardial oxygen consumption (MVO2) with its determinants in left ventricular hypertrophy in human beings is poorly understood. Therefore, thermodilution-derived coronary blood flow, MVO2 and left ventricular wall stress, obtained from simultaneous left ventricular M-mode echogram and pressure, were compared in 32 patients with various degrees of left ventricular hypertrophy. Patients were studied at rest and after mechanical load alteration with nitroglycerin or phenylephrine. Decreases in MVO2 (-5.7 +/- 0.8 ml/min; p less than 0.001) and the time integral of meridional ejection stress or shortening load (-1,297 +/- 152 X 10(3) dynes X s/cm2; p less than 0.001) were observed after nitroglycerin administration while increases in MVO2 (+5.5 +/- 0.7 ml/min; p less than 0.001) and shortening load (+1,412 +/- 137 X 10(3) dynes X s/cm2; p less than 0.001) were noted after phenylephrine. An index relating the change in MVO2 to the corresponding change in shortening load (SL), % delta MVO2/% delta SL, was significantly different in patients without (Group 1) and with (Group 2) clinical left ventricular failure. Left ventricular mass was similar in both groups. The mean % delta MVO2/% delta SL with phenylephrine in Group 1 (79.6 +/- 9.6) was greater than the index for Group 2 (35.5 +/- 6.1; p less than 0.005). With nitroglycerin, Group 2 patients exhibited a greater reduction in % delta MVO2/% delta SL (110.5 +/- 17.8) than Group 1 (54.0 +/- 9.4; p less than 0.01). In conclusion, in patients with left ventricular hypertrophy and dysfunction there appears to be a state of diminished coronary flow response to load augmentation. However, load reduction in patients with clinical left ventricular failure results in a more balanced relation between oxygen uptake and ejection stress.

Adult↗

Assessment of left ventricular mechanics in patients with asymptomatic aortic regurgitation: a two-dimensional echocardiographic study.

We describe a noninvasive method for determining end-systolic meridional and circumferential wall stress and left ventricular architecture as the ratio of muscle to cavity area. With this technique, which uses two-dimensional echocardiography and cuff-determined values for systolic blood pressure, we assessed wall stress and left ventricular architecture in 15 normal subjects and 15 asymptomatic patients with severe chronic aortic regurgitation at rest and after load manipulations with sublingual nitroglycerin. Resting end-systolic meridional and circumferential stress were increased in patients with aortic regurgitation (113.9 +/- 29 and 260 +/- 50.7 X 10(3) dynes/cm2) compared with those in normal subjects (85.6 +/- 15.4 and 214.1 +/- 28.4 X 10(3) dynes/cm2) (both p less than .01) and remained significantly greater after nitroglycerin. Meridional stress values obtained from two-dimensional echocardiographic studies correlated closely (r = .89) with values calculated from simultaneously recorded M mode echocardiograms. Ejection fraction in patients with aortic regurgitation and normal subjects were similar at rest (55 +/- 10% vs 59 +/- 6%) and were unchanged by nitroglycerin. In spite of the increased left ventricular mass in patients with aortic regurgitation (227 +/- 60 g vs 130 +/- 22 g in normal subjects), the mass-to-volume ratio and the ratio of muscle to cavity area in diastole in patients with aortic regurgitation were significantly lower than normal (0.90 +/- 0.23 vs 1.30 +/- 0.21 and 0.91 +/- 0.23 vs 1.11 +/- 0.18 [p less than .005 and p less than .02]). These differences were exaggerated after nitroglycerin, while concomitant changes in relative wall thickness were virtually undetected by M mode echocardiography. Thus this technique can be used for early recognition of afterload excess and changes in left ventricular architecture in patients with aortic regurgitation. Furthermore, the mean slopes of the circumferential stress-diameter and meridional stress-length lines, which represent load-independent indexes of myocardial contractile state, could be assessed and were similar in the group of patients with asymptomatic aortic regurgitation and normal subjects, indicating that overall myocardial contractility was still normal. We conclude that circumferential and meridional wall stress, myocardial contractility, and left ventricular architecture can be determined noninvasively. These measurements may prove to be useful in assessing patients with primary myocardial or valvular heart disease and determining their long-term management.

Adolescent↗

Quantitative assessment of growth and function of the cardiac chambers in the normal human fetus: a prospective longitudinal echocardiographic study.

We assessed the changes in cardiac chamber size, architecture and function in the normal fetus in a prospective, longitudinal, two-dimensional, and two-dimensionally directed M mode echocardiographic study. Serial echocardiograms were recorded in 16 normal fetuses at 4 week intervals from 20 weeks gestation to parturition. Fetal gestational age was assessed by biparietal diameter. Left ventricular, right ventricular, and left atrial chamber sizes and aortic diameter all increased linearly with age. The ratios of right and left ventricular diameter, left atrial to aortic diameters, and relative left ventricular wall thickness that we used as an index of short-axis left ventricular architecture remained constant. Fractional right ventricular and left ventricular wall thicknesses were similar both on echocardiograms and in postmortem hearts over the same range of gestational ages. In addition, postmortem right ventricular and left ventricular free wall weights were indistinguishable and contributed the same proportion to total heart weight throughout gestation. Left ventricular echocardiographic mass increased linearly from a mean of 0.86 +/- 0.09 to 7.47 +/- 2.43 g at term and corresponded closely with postmortem left ventricular weight. We conclude that (1) fetal cardiac chamber dimensions, wall thicknesses, and left ventricular mass increased with gestational age, (2) cardiac architecture in terms of the ratios of right ventricular/left ventricular diameters, left atrial/aortic diameters, and relative wall thickness remained constant, (3) right and left ventricular fractional shortening did not change with age, (4) left ventricular mass assessed echocardiographically corresponded closely with postmortem left ventricular weights in fetal hearts of similar gestational ages, and (5) the similarities between right and left ventricular sizes, wall thicknesses, and free wall weights in this study do not support the theory of right ventricular dominance in the human fetus.

Echocardiography↗

Quantitative assessment of right and left ventricular growth in the human fetal heart: a pathoanatomic study.

We quantitated the growth patterns of the normal fetal heart and the right and left ventricles from postmortem hearts obtained from 55 spontaneously aborted human fetuses from the completion of cardiogenesis to term. Fetal gestational age was assessed by menstrual history of the mother, crown-rump length, head circumference, and body weight and ranged from 8 to 40 weeks. Each heart was perfused and fixed at constant pressure and dissected to obtain right and left ventricular free wall, left ventricular, and total heart weights. Right and left ventricular free wall thicknesses were measured and the respective surface areas were calculated. The changes in each of these parameters with gestational age were examined by regression analysis. Total heart and right and left ventricular wall weights increased linearly with body weight, but exponentially with head circumference, crown-rump length, and menstrual history. Right and left ventricular free wall weights were similar throughout gestation and the percent that each contributed to total heart weight were constant at 29 +/- 2% and 30 +/- 2%, respectively. Right and left ventricular wall thicknesses did not differ significantly, increasing linearly with menstrual age, crown-rump length, head circumference, and body weight from 8 to 40 weeks. The surface areas of the right and left ventricular free walls that we used as an index of changing ventricular architecture were indistinguishable throughout the period of gestation studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The correlation of changes in systolic blood pressure with regional anatomical regression of hypertensive left ventricular hypertrophy in patients on chronic antihypertensive therapy (greater than 1 year): alpha-methyldopa compared to propranolol.

Twenty patients with mild to moderate hypertension and evidence of left ventricular hypertrophy (relative wall thickness greater than or equal to 0.45), who previously had not received either alpha-methyldopa or propranolol, were allocated at random to treatment with one or other of these drugs as monotherapy after a 2-week baseline period on no medication. Dosage was titrated until normotension was attained and patients were then maintained on this treatment for a year. Analysis of blood pressure measurements and echocardiograms taken before and during maintenance therapy showed that there were significantly correlated changes in systolic blood pressure and heart rate with left ventricular cavity and regional wall changes during chronic drug administration. In the alpha-methyldopa group there were significant correlations between changes in erect and supine systolic blood pressure and the posterior wall index, and in erect systolic blood pressure and left ventricular mass. In the propranolol group, there were significant correlations between changes in supine systolic blood pressure and interventricular septal thickness, and in erect heart rate and supine systolic blood pressure with the percentage change in internal diameter of the left ventricle. It is suggested that these observations may have important therapeutic implications for hypertensive patients with documented left ventricular hypertrophy.

Adult↗

Nongated cardiac magnetic resonance imaging: preliminary experience at 0.12 T.

Nongated cardiac magnetic resonance imaging (MRI) has been reported previously to be inadequate for obtaining diagnostic information. This study explored the role of pulse sequence in the degradation of the nongated cardiac image. Images of diagnostic quality were obtained by using single spin-echo sequences with a very short echo time (10-20 msec TE) on a 0.12-T developmental MR unit. Marked degradation of the image was noted with longer TEs, and it is concluded that the previous unfavorable reports using a nongated technique may have been due to the longer TEs used in other units. Short-TE technique was used to examine 34 patients with a variety of cardiac diseases. Eleven patients had ventricular aneurysms. These cases showed thinning of the myocardium, and four of them showed increased signal within the aneurysm, perhaps related to regionally slower blood flow. Twenty patients had enlargement of one or more cardiac chambers. Three of these patients had thrombus within an enlarged chamber, which was readily identified on MRI. Twelve patients had left ventricular hypertrophy that was concentric in 11. One patient demonstrated asymmetric septal hypertrophy. All four pericardial effusions were low in signal intensity, but this was related to the pulse sequence used. Six patients had extrinsic masses displacing the heart and distorting the chamber contour. One patient showed intracardiac invasion of tumor; this finding was not evident on the CT. One patient with ventricular septal defect (VSD) and corrected transposition was scanned. In addition to identifying the VSD and chamber hypertrophy, the malposition of the great vessels at the base of the heart was seen. Four postoperative patients were scanned; wire suture artifact did not preclude imaging. In conclusion, diagnostic information can be obtained from nongated cardiac images provided that the TE is very short (10-20 msec). Although quantitative functional data are not available from nongated images, qualitative and diagnostic information is possible and may suffice in certain circumstances.

Cardiomegaly↗

Mechanics of pulsus alternans in aortic valve stenosis.

Differences in the mechanics of strong and weak contractions during sustained pulsus alternans were studied in 4 patients with aortic valve stenosis (AS). No significant difference was observed between strong (S) and weak (W) beats in M-mode echographic end-diastolic minor-axis dimension or end-diastolic meridional wall stress. Peak systolic meridional stress (S:225 X 10(3) dynes/cm2; W:205 X 10(3) dynes/cm2), the time integral of left ventricular (LV) meridional systolic stress (S:5,000 X 10(3) dynes/cm2; W:4,500 X 10(3) dynes/cm2) and the area of a stress dimension loop (S:202 X 10(3) dyne/cm; W 165 X 10(3) dyne/cm) were all greater for strong beats. However, end-systolic meridional stress (S:100 X 10(3) dynes/cm2; W:115 X 10(3) dynes/cm2) and end-systolic minor-axis dimension (S:4.75 cm; W:5.0 cm) were significantly greater for weak beats. Stress-length relations, derived from resting and postnitroglycerin determinations, revealed higher end-systolic dimensions for weak beats at any level of limiting afterload, suggesting diminished contractile performance of weak beats. Additionally, fractional minor-axis shortening for weak beats was diminished, at any level of end-systolic stress, in comparison with that for strong beats. The results are supportive of theories suggesting alternating contractile performance during pulsus alternans.

Aortic Valve Stenosis↗

Myocardial oxygen consumption in left ventricular hypertrophy and its relation to left ventricular mechanics.

Alterations in left ventricular (LV) mechanics have significant effects on myocardial oxygen consumption (MVO2) as a result of changing LV pressure and dimensions. However, the effects of load alteration on MVO2 in the setting of LV hypertrophy and LV dysfunction have not been well characterized. Therefore, we examined changes in LV mechanics and MVO2 in 32 patients with varying degrees of LV hypertrophy and LV dysfunction before and after pharmacologic alteration of load. With phenylephrine or nitroglycerin-induced load alteration, changes in peak systolic meridional stress, mean systolic stress and the area of a stress-dimension loop all correlated modestly with changes in MVO2 (r = 0.66, 0.62, 0.63, respectively). However, changes in the time integral of LV ejection stress, or shortening load, were significantly correlated with changes in MVO2 (r = 0.88, p less than 0.001). In particular, load reduction results in a beneficial effect on MVO2. In addition, for a given change in LV systolic pressure, changes in shortening load (38 +/- 3.7%) were significantly greater than changes in tension-time index (13 +/- 1.4%), thus providing a sensitive marker of alteration of mechanical load. We conclude that physiologic alterations in mechanical load in normal persons as well as patients with LV hypertrophy are reflected in significant changes in the time integral of LV ejection stress. These changes in shortening load, mediated by changing LV pressure and dimension, are significantly related to changes in MVO2.

Adult↗

Echocardiographic assessment of left ventricular structure and function in hypertension. Methodology.

M-mode and two-dimensional echocardiography now provide an armamentarium of noninvasive techniques that permit assessment of left ventricular pump function, quantitation of afterload, a load-independent assessment of contractile state, and quantitation of pressure overload hypertrophy. Combined application of these methods to problems in the assessment of hypertensive heart disease can clarify both disease mechanisms and therapeutic effects by identifying the contributions of changes in myocardial mass, alterations in contractile state and variations in afterload to a given phenomenon.

Adaptation, Physiological↗

Role of nitroglycerin in effort angina.

The use of nitroglycerin in the treatment of effort angina has two facets (1) relief of established episodes of angina, and (2) prophylaxis to enhance exercise capacity. To produce relief of angina in a substantial proportion of patients, a nitrate preparation must begin to have an effect within two minutes or less. Such rapid onset has been documented only with sublingual nitroglycerin, inhaled amyl nitrate, and two new preparations: nitroglycerin spray and sustained release transmucosal nitroglycerin. Prophylactic effects of nitrates are best assessed and compared using double-blind, placebo-controlled exercise testing at multiple time points after the administration of carefully titrated matched doses. A bicycle ergometer protocol devised at the National Heart, Lung and Blood Institute has been widely used for this purpose and permits comparison of various "long-acting" nitrates at doses that produce peak effects comparable to conventional doses of sublingual nitroglycerin. Oral isosorbide dinitrate and 2 percent nitroglycerin ointment enhance effort tolerance for up to three hours after administration, whereas sustained release transmucosal nitroglycerin produces such effects for up to five hours. Similar clinical efficacy data are lacking for the new cutaneous nitroglycerin patches. In clinical use, larger doses of nitroglycerin in any form may produce more marked and prolonged prophylactic effects. Despite the availability of multiple new antianginal agents of the calcium antagonist and beta blocker types, nitroglycerin continues to be a mainstay of antianginal therapy and is likely to remain so for the foreseeable future. However, new high dose prolonged effect regimens raise important questions about the frequency and clinical significance of nitrate tolerance.

Adrenergic beta-Antagonists↗

Determinants of circulatory response to intravenous hydralazine in congestive heart failure.

To determine whether the circulatory response to hydralazine in heart failure is influenced by initial hemodynamic status or left ventricular (LV) chamber size, 28 patients with chronic LV dysfunction were studied. Hemodynamic measurements and echocardiographic LV end-diastolic dimension were correlated with the response to 20 mg of intravenous hydralazine and to a dose titrated in each patient to reduce systemic resistance by greater than or equal to 20%. Hydralazine, 20 mg, decreased systemic resistance from 23 +/- 8 to 18 +/- 8 U (p less than 0.01) and increased the cardiac index from 2.0 +/- 0.5 to 2.5 +/- 0.6 liters/min/m2 (p less than 0.01) and the stroke work index from 21 +/- 11 to 24 +/- 9 g . m/m2 (p less than 0.05). Titrating the dose to decrease systemic resistance by greater than or equal to 20% increased the cardiac index further to 2.7 +/- 0.6 liters/min/m2 and the stroke work index to 32 +/- 9 g . m/m2. The change in systemic resistance produced by 20 mg of hydralazine correlated only with initial systemic resistance (r = 0.53), suggesting that vascular response to hydralazine is a direct function of initial vascular resistance. The percentage change in stroke work index produced by 20 mg of hydralazine correlated directly with indexes of LV preload-end-diastolic wall stress (r = 0.69) and pulmonary wedge pressure (r = 0.43) and inversely with stroke work index (r = -0.49), an index of ventricular work. Similar but less close correlations were observed when the dose of hydralazine was titrated. The hemodynamic response to hydralazine did not correlate with LV end-diastolic dimension or right atrial pressure. Thus, vascular response to moderate doses of hydralazine is related to initial systemic vascular resistance. LV pump response is related to the level of initial LV pump dysfunction but not to LV chamber size or right atrial pressure.

Female↗

Anatomic validation of left ventricular mass estimates from clinical two-dimensional echocardiography: initial results.

We performed a prospective anatomic validation study to determine the accuracy of left ventricular (LV) mass estimates from clinical two-dimensional echocardiographic (2-D echo) studies. In 21 subjects, antemortem 2-D echo LV mass determinations were compared with anatomic LV weight by postmortem chamber dissection. Major cardiac diagnoses included anatomic LV aneurysm in four, status post aneurysmectomy in one, transmural myocardial infarction in seven, congestive cardiomyopathy in five, rheumatic mitral disease in two, chronic severe mitral or aortic regurgitation in three, amyloid heart in two, and normal heart in three. Marked right-heart dilatation was present in 11 patients and LV thrombus in four. Regression equations derived in vitro for each 2-D echo instrument were used to correct LV mass estimates based on a short-axis, area-length method: uncorrected LV mass = 1.055 x k x 5/6 (AtLt - AcLc) + b, where At = total short-axis LV image area at the high papillary muscle level, Lc = endocardial LV length, k = an instrument-specific regression slope and b = an instrument-specific intercept. LV mass by 2-D echo correlated extremely well with actual LV weight (r = 0.93 slope = 0.85, SEE = 31 g, range 77-454 g). In contrast, M-mode echocardiographic LV mass estimates were less reliable (r = 0.86, SEE = 59 g) in these markedly distorted hearts. These 2-D echo LV mass results compare favorably with reported results from biplane angiography and M-mode echocardiography in more symmetric hearts. Thus, regression-corrected 2-D echo may be the method of choice for determining LV mass in man.

Echocardiography↗

Reliable estimation of peak left ventricular systolic pressure by M-mode echographic-determined end-diastolic relative wall thickness: identification of severe valvular aortic stenosis in adult patients.

In compensated hearts, left ventricular systolic pressure (LVSP) can be estimated from the ratio of LV wall thickness to chamber radius (RWT). To determine the clinical value of such estimates, we examined echocardiography RWT in an unscreened series of 81 individuals with aortic valve disease, hypertension, or normal hearts. Despite the presence, in many subjects, of symptoms of congestive heart failure, reduced ejection fraction, or coronary disease, end-diastolic RWT (RWTD) correlated well with peak LVSP (r = 0.77); 45 of 55 patients with LVSP greater than or equal to 140 mm Hg had RWTD greater than or equal to 0.45, while 26 of 26 with LVSP less than 140 mm Hg had lower values (p less than 0.005). RWTD was greater than or equal to 0.50 in 30 of 34 patients with LVSP greater than or equal to 180 mm Hg and in 6 of 21 with LVSP 140 to 180 mm Hg. RWTD correctly estimated LVSP range in 26 of 27 severe aortic stenosis (AS) patients and, combined with echocardiographic aortic valve calcification, correctly recognized the presence or absence of severe AS in 99% of the series. The RWTD for any given LVSP was higher in patients on antihypertensive treatment and lower in patients with severe aortic regurgitation. In contrast to series based on patients with normal LV function, end-systolic RWT correlated poorly with LVSP.

Adult↗

Repolarization abnormalities of left ventricular hypertrophy. Clinical, echocardiographic and hemodynamic correlates.

To evaluate the clinical significance of ECG depolarization abnormalities of left ventricular hypertrophy, ECG findings were related to echocardiographic or autopsy left ventricular mass, geometry and function as well as hemodynamic overload, in a heterogeneous population of 161 patients. ST depression and asymmetric T wave inversion were present in 21/107 patients not receiving digitalis (19%) and in 33/54 (61%) receiving digitalis. In patients not receiving digitalis their prevalence increased linearly from 0% (0/31) with LV mass less than or equal to 100 grams to 100% (8/8) with LV mass over 400 grams (p less than 0.001). Patients taking digitalis manifested "strain" commonly despite a normal LV mass (4/14, 28%), but even more frequently with an LV mass over 200 grams (27/40, 68%) (p less than 0.05). In the absence of digitalis, repolarization abnormalities were also significantly associated with a reduced ejection fraction (8/17 or 47% versus 8/83 or 10%; p less than 0.001), increased LV internal diameter (9/18 or 50% versus 12/89 or 13%; p less than 0.01), and systolic blood pressure over 140 mm Hg (9/29 or 31% versus 7/61 or 11%; p less than 0.05). Increased thickness of the LV wall was not significantly associated with LV "strain" (p = 0.1). In this population, LV "strain" alone performed as well as other single or combined ECG criteria in the recognition of LVH (sensitivity 52%, specificity 95%). Thus, in the absence of digitalis, repolarization abnormalities are a highly useful ECG sign of LVH, despite numerous other factors capable of causing indistinguishable abnormalities.

Adolescent↗