[The dispersion of ventricular repolarization diagnosed by Holter: limitations and possibilities].
Explore the source record for details and available documents.
Electrocardiography, Ambulatory↗
Biomedical subjects
C Lazzeri
Publications and source records attributed to C Lazzeri.
TCL1 is overexpressed in patients affected by adult T-cell leukemias.
Among mature postthymic T-cell leukemias, adult T-cell leukemia (ATL) has characteristic clinicopathological entities. The association with the human T-cell leukemia/lymphotropic virus type I is one of the distinctive etiopathogenetic features of this disease. However, unlike other acute transforming retroviruses, the human T-cell leukemia/lymphotropic virus type I lacks an oncogene within its genome. Other human postthymic leukemias, such as T-prolymphocytic leukemias, involve mostly the CD4 cellular subset and share many similarities to ATLs (aggressive course, cutaneous involvement, CD4+, CD29+, CD45RA- phenotype, and alpha-naphthyl-acetate esterase positivity). A chromosomal rearrangement at 14q32.1, involved in translocations or inversions with either the alpha/delta locus [t(14;14)(q11;q32.1), inv14(q11;q32.1)], or the beta-chain locus of the T-cell receptor [t(7;14)(q35;q32.1)] is found. These rearrangements disregulate a gene, TCL1, located at the 14q32.1 region, that we show is physiologically expressed in CD4/CD8 double-negative thymocyte cells, but not in more differentiated CD4+ and CD8+ subpopulations. Here, using molecular and immunocytochemical analysis, we report that TCL1 is also overexpressed in 10 of 10 ATL specimens, indicating that this gene may play an important role in the pathogenesis of this disease.
Adult↗
Cerebral autoregulation in patients with cirrhosis and ascites. A transcranial Doppler study.
BACKGROUND/AIMS: Patients with cirrhosis and ascites usually show alterations of systemic hemodynamics and are thus prone to develop arterial hypotension, which might result in cerebral hypoperfusion if cerebral autoregulation is impaired. METHODS: We evaluated cerebral autoregulation in 15 patients with cirrhosis and ascites and 15 healthy subjects by monitoring mean blood flow velocity in the middle cerebral artery and arterial pressure during supine rest and passive tilting. RESULTS: Tilt provoked a drop of arterial pressure in both groups. Control subjects had a prompt recovery of mean flow velocity and a progressive recovery of arterial pressure, so that, after 120 s, both parameters had returned to baseline: at 20 s the recovery of flow velocity was faster (p<0.01) than that of blood pressure. By contrast, patients with cirrhosis had a delayed and incomplete recovery of both parameters (p<0.01 vs healthy subjects). In eight patients, the recovery of mean flow velocity paralleled that of arterial pressure, indicating an impaired cerebral autoregulation. These patients had a worse liver function, a higher cardiac index and lower peripheral resistance. CONCLUSIONS: Cerebral autoregulation is often impaired in patients with cirrhosis and ascites. These patients can develop cerebral hypoperfusion if arterial pressure falls abruptly.
Aged↗
Parallel increase in carotid, brachial and left ventricular cross-sectional areas in arterial hypertension.
Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.
Adult↗
Autonomic regulation of heart rate and QT interval in nonalcoholic cirrhosis with ascites.
BACKGROUND/AIMS: Autonomic neuropathy, as indicated by alterations in standard cardiovascular tests, is frequently encountered in cirrhosis. We investigated the autonomic modulation of the heart in nonalcoholic cirrhosis with ascites by evaluating the 24-hour heart rate variability (HRV), a powerful noninvasive tool to assess the sympathovagal balance of the heart. METHODS: Low (LF) and high frequency (HF) components and their ratio, and time domain indexes of HRV were evaluated in 24-hour, daytime and nighttime periods in 12 patients and 12 healthy subjects, together with the conventional and dynamic QT interval. RESULTS: Cirrhotic patients had values of the mean RR interval and frequency domain indexes in the whole 24-hour period similar to those of healthy subjects, despite higher than normal plasma norepinephrine levels. Patients also showed lower LF and higher HF values than controls during the day, a reduction in time domain indexes, and no circadian rhythm of frequency domain indexes. QT parameters were similar in the 2 groups, but patients had a blunted QT rhythm and a reduced QT variability. CONCLUSIONS: Patients with nonalcoholic cirrhosis and ascites have an impaired autonomic regulation of the heart, which involves both the sympathetic and the parasympathetic branches of the autonomic nervous system.
Aged↗
Urinary endothelin-1 excretion is enhanced by low-dose infusion of brain natriuretic peptide in normal humans.
To evaluate the functional relationship between cardiac natriuretic peptides and endothelin-1 within the human kidney, we studied the effects exerted by infusion of brain natriuretic peptide on urinary endothelin-1 excretion. We studied twice in a single-blind manner five normal volunteers who received a constant infusion of 5% dextrose (250 mL/h) or human brain natriuretic peptide-32 at a dose of 4 pmol/kg per minute. Blood samples were drawn at intervals for measurement of hematocrit and concentrations of creatinine, electrolytes, brain natriuretic peptide, and endothelin-1. Urine was collected an intervals for measurement of flow rate and concentrations of creatinine, sodium, cGMP, and endothelin-1. Blood pressure and heart rate were measured every 15 minutes. Placebo administration did not change blood pressure, heart rate, or any of the other parameters measured in plasma and urine. As expected, brain natriuretic peptide infusion caused significant increases in its own plasma levels (basal versus peak levels [mean +/- SD], 1.45 +/- 0.20 versus 50.5 +/- 6.0 pmol/L, P < .01), in urinary cGMP (0.75 +/- 0.16 versus 1.92 +/- 0.81 fmol/min, P < .05), and in urinary sodium excretion (140.0 +/- 38.7 versus 624.2 +/- 181.6 mumol/min, P < .01). In addition, it caused an increase in urinary endothelin-1 excretion (4.32 +/- 2.11 versus 19.67 +/- 9.52 fmol/min, P < .05), without modifying plasma endothelin-1, blood pressure, heart rate, creatinine clearance, and urinary flow rate. Our data indicate that brain natriuretic peptide, at plasma levels comparable to those observed in patients with heart failure, causes a significant increase in urinary but not plasma endothelin-1, thus demonstrating a functional link between cardiac natriuretic peptides and renal release of endothelin-1.
Adult↗
Cardiovascular and renal effects of low-dose atrial natriuretic peptide in compensated cirrhosis.
OBJECTIVES: Patients with cirrhosis and ascites have high plasma levels of atrial natriuretic peptide (ANP). Pharmacological doses of this hormone usually worsen systemic hemodynamics of cirrhotic patients. We assessed whether ANP influences cardiovascular homeostasis and renal function in patients with compensated cirrhosis at plasma levels comparable to those observed in patients with cirrhosis and ascites. METHODS: Radionuclide angiocardiography was performed in eight compensated cirrhotic patients during placebo (three periods of 15 min each) and ANP infusion (2, 4, and 6 pmol/kg.min for 15 min each), together with appropriate blood and urine sampling, to evaluate left ventricular diastolic, systolic, and stroke volume, heart rate, cardiac output, arterial pressure, peripheral vascular resistance, creatinine clearance, urinary sodium excretion, plasma renin activity, plasma aldosterone, norepinephrine and hematocrit. RESULTS: The infusion increased plasma ANP up to levels (52.03 +/- 2.29 pmol/L) comparable with those observed in 35 patients with ascites (46.42 +/- 1.57 pmol/ L). This increment was associated with significant reductions in left ventricular end diastolic volume, stroke volume, cardiac index (from 3.7 +/- 0.7 to 3.1 +/- 0.5 L/min.m2, p < 0.05) and mean arterial pressure (from 96.7 +/- 6.5 to 88.5 +/- 9.5 mmHg, p < 0.05), while heart rate and hematocrit significantly increased. Peripheral vascular resistance did not change. These hemodynamic effects occurred despite significant increases in plasma renin activity and norepinephrine. ANP also induced increases in creatinine clearance, urinary sodium excretion, and fractional sodium excretion. CONCLUSIONS: Low-dose ANP affected cardiovascular homeostasis and renal sodium handling in compensated cirrhosis, suggesting that this hormone may be involved in the pathophysiology of systemic hemodynamic and renal functional abnormalities of cirrhosis.
Aldosterone↗
Blunted natriuretic response to low-dose brain natriuretic peptide infusion in nonazotemic cirrhotic patients with ascites and avid sodium retention.
Patients with cirrhosis and ascites have high plasma levels of atrial (ANP) and brain (BNP) natriuretic peptides, two cardiac hormones released by the atria and ventricles, respectively. We evaluated renal hemodynamics, sodium excretion, and intrarenal sodium handling (lithium clearance method) in seven cirrhotic patients with ascites and avid sodium retention before, during, and after the infusion of synthetic human BNP, at the dose of 4 pmol/kg.min for 1 hour, which has been shown to increase renal plasma flow, glomerular filtration rate (GFR), and sodium excretion in healthy subjects without affecting systemic hemodynamics. Plasma BNP levels were 7.31 +/- 0.85 pmol/L in baseline conditions, and increased to 33.60 +/- 2.96 pmol/L at the end of the infusion (P < .01 vs. baseline). Urinary excretion of guanosine 3',5'-cyclic monophosphate (cGMP) also significantly increased during the infusion, indicating stimulation of natriuretic peptide receptors by BNP. BNP administration did not modify renal plasma flow, GFR, sodium excretion or tubular sodium reabsorption to any appreciable extent. Arterial pressure heart rate, plasma norepinephrine, and plasma renin activity (PRA) where also unchanged, whereas plasma aldosterone concentration showed a significant, 35% reduction at the end of the postinfusion period, ruling out the possibility that BNP-induced vasodilation might be responsible for failure of the peptide to induce a natriuretic response. Overactivity of antinatriuretic factors is probably the main determinant of the blunted natriuretic effect of BNP in these patients.
Adult↗
Systemic hemodynamics and renal function during brain natriuretic peptide infusion in patients with essential hypertension.
We assessed the cardiovascular and renal effects of human brain natriuretic peptide (BNP) infused at a dose inducing an increase in plasma BNP to pathophysiologic levels, in eight hypertensive patients in a randomized, placebo-controlled, cross-over study. Left ventricular performance, cardiac output (echocardiography), heart rate, arterial pressure, glomerular filtration rate (GFR; creatinine clearance), sodium excretion, intrarenal sodium handling (lithium clearance method), and urine flow rate were measured in the infusion and postinfusion periods (1 h each), together with plasma BNP and the urinary excretion rate of cGMP. Plasma BNP levels increased from 2.90 +/- 0.74 to 36.43 +/- 5.51 pmol/L (P < .01) at the end of the infusion and were still elevated at the end of the postinfusion period (7.03 +/- 1.41 pmol/L, P < .05). The urinary excretion of cGMP was also significantly higher during BNP infusion. Left ventricular performance, cardiac output, arterial pressure, and peripheral vascular resistance were not affected by BNP. Peptide infusion induced a significant increase in GFR (placebo, 115 +/- 24; BNP, 147 +/- 19 mL/min), sodium excretion (placebo, 129 +/- 40; BNP, 243 +/- 60 mumol/min), and urine flow rate. All these effects were observed also in the postinfusion period. The natriuretic effect of BNP was attributable to both an increase in filtered sodium load and a reduction of distal sodium reabsorption. These results suggest that BNP may contribute to maintain renal function and sodium excretion in patients with essential hypertension.
Adult↗
Cardiovascular function during brain natriuretic peptide infusion in man.
To investigate the cardiovascular effects of pathophysiological levels of brain natriuretic peptide (BNP), 7 healthy subjects were submitted to equilibrium radionuclide angiocardiography in baseline conditions and during BNP infusion at increasing doses (4, 8, 10 and 12 pmol/kg.min for 20 min each). BNP induced a progressive, significant reduction in left ventricular end diastolic volume, stroke volume and end systolic volume and an increase in ejection fraction and heart rate. Cardiac output, arterial pressure and peripheral vascular resistance were unchanged. Activation of the sympathetic nervous system, as indicated by the significant increase in plasma norepinephrine levels, probably played a contributory role in the maintenance of cardiovascular homeostasis. These results indicate that BNP, at pathophysiological plasma concentrations, influences cardiovascular homeostasis in man.
Adult↗
Cardiovascular effects of brain natriuretic peptide in essential hypertension.
We evaluated the cardiovascular effects of pathophysiological plasma levels of brain natriuretic peptide in seven patients with mild to moderate essential hypertension by performing equilibrium radionuclide angiocardiography at baseline and during brain natriuretic peptide infusion at increasing doses (4, 8, 10, and 12 pmol/kg per minute for 20 minutes each). Brain natriuretic peptide induced a progressive reduction of left ventricular end-diastolic volume (from 107.5 +/- 10.3 to 89.0 +/- 11.0 mL at the end of all infusion periods) and end-systolic volume, whereas stroke volume did not show any significant change (from 64.9 +/- 5.9 to 62.7 +/- 7.8 mL). Cardiac output, arterial pressure, and peripheral vascular resistance did not change significantly. The lack of effects on systemic hemodynamics was probably due to compensatory activation of the sympathetic nervous system, as indicated by the significant increase in plasma norepinephrine levels (from 1.75 +/- 0.18 to 2.19 +/- 0.21 nmol/L), heart rate (from 68 +/- 6 to 81 +/- 6 beats per minute), peak ejection rate, and peak filling rate. These results indicate that brain natriuretic peptide, at the pathophysiological plasma concentrations reached in this study, influences cardiovascular homeostasis mainly by reducing cardiac preload.
Aged↗
Acute effects of physiological increments of brain natriuretic peptide in humans.
To investigate the effects of physiological increases in plasma brain natriuretic peptide concentration in humans, we studied six healthy volunteers who received incremental infusions (0.25 pmol/kg per minute in the first hour and 0.50 pmol/kg per minute in the second) of synthetic human brain natriuretic peptide-32 in a placebo-controlled, crossover study. Peptide plasma levels were 1.69 +/- 0.39 pmol/L at baseline and rose 1.5- and 3-fold with the lower and higher doses, respectively. These values were within the normal range and also comparable to those reported in patients with mild essential hypertension. The urinary excretion rate of cGMP also increased during brain natriuretic peptide infusion, indicating stimulation of natriuretic peptide receptors. Peptide administration induced a significant 1.7-fold increase in urinary sodium excretion without affecting renal plasma flow (para-aminohippurate clearance), glomerular filtration rate (creatinine clearance), and urine flow rate. Fractional proximal sodium reabsorption (lithium clearance method) was unchanged, and fractional distal sodium reabsorption significantly decreased. Brain natriuretic peptide caused no changes in arterial pressure, heart rate, hematocrit, and serum proteins, but it exerted an inhibitory effect on the renin-aldosterone axis, as indicated by the significant 50% or more decrease of plasma renin activity and urinary excretion rate of aldosterone. These results suggest that brain natriuretic peptide may be involved in the overall regulation of body fluid and cardiovascular homeostasis in humans, mainly through its natriuretic and endocrine effects.
Adult↗
Plasma levels of natriuretic peptides during ventricular pacing in patients with a dual chamber pacemaker.
The mechanism(s) responsible for the release of brain natriuretic peptide (BNP), a cardiac hormone of ventricular origin, are still not completely understood. We measured plasma atrial natriuretic peptide (ANP) and BNP in 15 subjects (10 men, mean age 67 +/- 3 years) with a dual chamber pacemaker and unimpaired heart function during ventricular pacing, which is known to induce an increase in atrial pressure and plasma ANP concentration. Under ECG monitoring, all subjects received sequential atrioventricular pacing for 30 minutes and ventricular pacing for 30 minutes, at the same rate of 80 beats/min. Arterial pressure and plasma BNP and ANP levels were measured every 10 minutes throughout the study. Ventricular pacing led to atrioventricular dissociation in eight subjects and to retrograde ventriculo-atrial conduction in seven. Arterial pressure remained unchanged in all subjects. In the group with atrioventricular dissociation, plasma ANP increased from 10.14 +/- 0.58 to 16.72 +/- 0.92 fmol/mL at the 60th minute (P < 0.0001), whereas plasma BNP did not change at all (from 1.26 +/- 0.07 to 1.16 +/- 0.09 fmol/mL). In the group with retrograde conduction, plasma ANP concentration doubled (from 10.95 +/- 1.66 to 21.40 +/- 1.51 fmol/mL, P < 0.0001), BNP increased 1.5-fold (from 1.16 +/- 0.06 to 1.64 +/- 0.14 fmol/mL, P < 0.001), and the ANP:BNP ratio augmented from 10:1 to 13.4:1. These results indicate that the release of ANP and BNP is regulated by different mechanisms, supporting the view that there is a dual natriuretic peptide system, comprising ANP from the atria and BNP from the ventricles.
Aged↗
Cardiovascular and renal effects of low dose brain natriuretic peptide infusion in man.
We evaluated the effects of pathophysiological levels of human brain natriuretic peptide (BNP), a recently identified cardiac hormone with natriuretic activity, by determining the hemodynamic and renal responses to low dose infusion (4 pmol/kg.min for 1 h, from 1500-1600 h) of human synthetic BNP in five healthy volunteers in a randomized placebo-controlled crossover study. Compared to placebo, BNP induced significant increases in effective renal plasma flow (para-aminohippurate clearance), glomerular filtration rate (creatinine clearance), urine flow rate, and sodium excretion without affecting blood pressure, heart rate, cardiac output (echocardiographic method), peripheral vascular resistance, PRA, plasma aldosterone, or plasma norepinephrine to any significant extent. Exploration of segmental sodium handling by the lithium clearance technique showed that the natriuretic effect of BNP was due to both an increase in filtered sodium load and a reduced distal sodium reabsorption. These results indicate that the high plasma BNP levels observed in disease states, such as heart failure, may contribute to the regulation of renal hemodynamics and sodium excretion.
Adult↗
Plasma levels of brain natriuretic peptide in healthy subjects and patients with essential hypertension: response to posture.
1. To examine whether posture-induced changes in central volume affect brain natriuretic peptide secretion, plasma levels of human brain natriuretic peptide-32-like immunoreactivity (hBNP-32-li) were measured by radioimmunoassay in 11 healthy subjects and 20 patients with essential hypertension after 15 min supine, 15 min sitting and 15 min with the legs raised at 60 degrees, together with plasma atrial natriuretic peptide concentration, plasma renin activity and plasma aldosterone concentration. 2. In the supine position, the plasma hBNP-32-li level was 1.57 +/- 0.10 fmol/ml in healthy subjects and significantly higher in hypertensive patients (2.39 +/- 0.13 fmol/ml, P < 0.001). In both groups, plasma hBNP-32-li level significantly (P < 0.001) decreased when sitting (normotensive, 1.22 +/- 0.08 fmol/ml; hypertensive, 1.85 +/- 0.15 fmol/ml, P < 0.001 versus normotensive) and increased again after leg raising (normotensive, 2.13 +/- 0.12 fmol/ml; P < 0.002 versus resting; hypertensive, 2.84 +/- 0.16 fmol/min, P < 0.001 versus resting, P < 0.025 versus normotensive). 3. The plasma atrial natriuretic peptide concentration showed similar behaviour to the plasma hBNP-32-li, whereas plasma renin activity and plasma aldosterone concentration increased during sitting and decreased during leg raising in both healthy subjects and hypertensive patients, who had significantly higher plasma aldosterone levels when supine and sitting.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Dopamine and sympathoadrenal activity in man.
The sympathetic adrenal (SA) activity can be modulated by dopamine (DA) through D2 receptors. In man, using D2 antagonists, it has been demonstrated that endogenous DA plays an inhibitory modulation of the SA system during high degree of SA activation. D2 agonists are able to induce a decrease in norepinephrine (NE) release either in vitro or in vivo. This effect leads, in vivo, to a decrease in blood pressure (BP) and to an activation of arterial baroreceptors. Therefore, in vivo, the D2 mediated inhibition of epinephrine (E) release, which is clearly demonstrated in vitro, is overwhelmed by the baroreceptor-mediated activation of the splachnic nerve. As a consequence, the in vivo administration of D2 agonists can induce a different effect on the net peripheral sympathetic tone of an organ, depending on the balance between the degree of the baroreceptor-mediated sympathetic activation and the inhibitory D2-mediated inhibition of NE release at the tissue level. In the present paper we investigated the in vivo effect of placebo (PL) or acute oral bromocriptine (BC) administration on plasma CA and on the cardiac sympatho-vagal balance of 7 normal volunteers, as assessed by power spectral analysis of heart rate (HR) variability (autoregressive method), either in resting or sitting position. Low frequency (LF) and high frequency (HF) components, both expressed in normalized units (nU), and LF/HF ratio were calculated. BC caused a decrease in BP, plasma NE and no change in HR in resting and sitting position. Plasma E increased in sitting position. At the heart level, after BC, we observed, during rest, an increase in LF and LF/HF ratio and a decrease in HF while in sitting position LF did not increase further. These data show that BC, while reducing BP through a decrease of plasma NE, increases LF/HF ratio (sympathetic tone) without any change in heart rate. These data seem to confirm that BC causes an inhibitory modulation of the SA system acting predominantly at the periphery through D2 presynaptic receptors.
Adrenal Medulla↗
[Brain natriuretic peptide].
Brain natriuretic peptide (BNP) is a cardiac hormone with a spectrum of activities quite similar to those of atrial natriuretic peptide (ANP), including diuretic, natriuretic, hypotensive and smooth muscle relaxant activities. These effects are due to the stimulation of guanylate cyclase-linked natriuretic peptide receptors, leading to an increase in cyclic GMP concentration in target cells. BNP has a lower affinity than ANP for C (clearance) receptors, and is less susceptible to degradation by neutral endopeptidase-24.11, resulting in a longer half-life. In the kidney, BNP increases the glomerular filtration rate and inhibits sodium reabsorption in the distal tubule. It also inhibits the release of renin and aldosterone. Unlike ANP, produced by the atria, BNP is mainly synthesized and released into circulation by the left ventricle and is therefore influenced by stimuli involving this cardiac chamber, such as an increase in arterial pressure, left ventricular hypertrophy and dilation. Plasma BNP levels are very low in healthy subjects, and respond modestly, although significantly to physiological stimuli such as changes in posture or sodium intake. In contrast, plasma BNP concentrations increase in disease states such as cirrhosis with ascites, hypertension, chronic renal failure, acute myocardial infarction and congestive heart failure. In the latter condition, plasma BNP concentration is a reliable prognostic index. Evidence obtained by administering BNP to healthy subjects and hypertensive patients suggests that BNP, at physiological and pathophysiological plasma concentrations, markedly influences cardiovascular homeostasis, mainly due to its effects on sodium excretion and the renin-aldosterone axis.
Animals↗
[Lipoprotein(a): genetic marker of precocious myocardial infarction].
Since an elevated serum concentration of lipoprotein(a) [Lp(a)] associated with a positive family history of premature myocardial infarction (PMI), would support the hypothesis that Lp(a) is a genetic risk factor for atherosclerosis, we measured serum levels in subjects from families with a history of PMI and compared them to those in a group of healthy control subjects. Twenty-five males (average age 39 +/- 16 years) and 9 females (average age 42 +/- 14 years) who had at least one blood relative affected by PMI were included in the study; 20 males (average age 41 +/- 11 years) and 10 females (average age 37 +/- 13 years) served as control subjects. Serum cholesterol, triglyceride, HDL-cholesterol, apo A1, apo B100 and Lp(a) concentrations were measured in both groups. The statistically significant higher prevalence of elevated Lp(a) levels (> 30 mg/dL) in the PMI group (p < 0.05) is attributable to the higher prevalence of PMI males with elevated Lp(a) levels. Pedigree studies disclosed a family distribution of coronary heart disease compatible with the hypothesis of a segregation of a dominant character for PMI risk. Because serum Lp(a) concentration is inherited with a Mendelian codominant pattern, we conclude that our data strongly support the hypothesis of a correlation between excess Lp(a) and coronary atherosclerosis.
Adult↗