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H Schunkert

Publications and source records attributed to H Schunkert.

At least 19 recordsLinked to original sources
PubMed2000

[ACE gene polymorphism and cardiovascular diseases].

The angiotensin converting enzyme (ACE) is an integral part of enzymatic cascades leading to generation of angiotensin II as well as degradation of bradykinin. For this reason, it represents an important part for the metabolism of 2 vasoactive peptides. Early in this decade, convincing experimental evidence demonstrated the induction of this enzyme in several pathophysiological conditions including myocardial infarction and left ventricular hypertrophy. In parallel, a deletion/insertion (D/I) polymorphism of the human ACE gene was discovered that was related to 14 to 50% of the interindividual variance of serum ACE activity. More recently, this polymorphism was implicated in the pathogenesis of a variety of cardiovascular disorders including myocardial infarction, left ventricular hypertrophy, hypertension as well as nephropathy.

Chromosome Deletion↗
PubMed2000

Evaluation of three polymorphisms in the promoter region of the angiotensin II type I receptor gene.

BACKGROUND: Angiotensin II induces vasoconstriction and growth via stimulation of the AT1 receptor. A genetic variant (+1166A/C) in the 3' untranslated region of this gene had been found to be associated with arterial hypertension, aortic stiffness and coronary artery disease. OBJECTIVE: In order to evaluate further the potential implications of the genetic variability of the AT1 gene we explored three newly characterized single nucleotide polymorphisms (SNPs) in its promoter in a Caucasian population-based sample (n = 623). One of these (-2228G/A) is in complete linkage disequilibrium with six additional SNPs in the region such that, indirectly, potential functional implications of these sites were assessed as well. For comparison, we genotyped the previously described +1166A/C variant RESULTS: The allele frequencies of the -2228G/A, -1424C/ G and -521 C/T SNPs were 0.82/0.18, 0.963/0.037 and 0.64/0.36, respectively. Statistical analysis by one-factor ANOVA revealed no significant relationship of any allele, genotype or haplotype with age, sex, body mass index, heart rate, systolic or diastolic blood pressure, hypertension, the intake of antihypertensive medication or left ventricular mass. Likewise, renin, angiotensinogen, angiotensin-converting enzyme, aldosterone or atrial natriuretic peptide levels were not found to be associated with any of these SNPs. Surprisingly, the -2228 A allele was found to be overrepresented in subjects with diabetes mellitus (n = 25, P = 0.006). However, this result could not be confirmed when additional individuals with diabetes mellitus (n = 45) were analysed. A weak linkage disequilibrium was observed between the -2228 A allele and the +1166 C allele (chi2 1 3.1; P = 0.010). CONCLUSION: From the present data it is unlikely that any one of the nine newly characterized SNPs in the promoter region of AT1 gene is associated with arterial hypertension.

Aged↗
PubMed2000

Comparative coronary anatomy in six twin pairs with coronary artery disease.

OBJECTIVE: To compare the coronary anatomy and the location of coronary lesions in monozygotic and dizygotic twin pairs affected with coronary artery disease. DESIGN: Coronary angiographic findings were compared with respect to the distribution of coronary blood supply and the location of coronary lesions. MAIN OUTCOME MEASURES: Distribution of coronary blood supply, diameters and length of proximal coronary arteries. RESULTS: The lumen diameters of the left main coronary artery, the left anterior descending coronary artery, the circumflex artery, and the right coronary artery, as well as the lengths of the left main coronary artery, showed similar variability within monozygotic and dizygotic twin pairs. With respect to the dominance pattern of coronary blood supply, two of three monozygotic twin pairs differed, while all dizygotic twin pairs were concordant. Concordant and discordant locations of stenoses were found with similar frequency in monozygotic and dizygotic twin pairs. CONCLUSIONS: The dominance pattern of coronary blood supply and the location of coronary lesions are not strictly hereditary. The high concordance of premature coronary artery disease found in monozygotic twin pairs may largely be related to factors that are independent of the macroanatomic distribution of the coronary blood supply.

Adult↗
PubMed2000

Evaluation of the aldosterone synthase (CYP11B2) gene polymorphism in patients with myocardial infarction.

Left ventricular remodeling after myocardial infarction involves activation of the renin-angiotensin-aldosterone system. Recently, the biallelic -344T/C polymorphism of the aldosterone synthase gene was associated with increased aldosterone levels, arterial hypertension, diastolic dysfunction, and left ventricular dilatation. We hypothesized that this polymorphism may also affect left ventricular geometry and function after myocardial infarction. By using a standardized questionnaire, as well as anthropometric and echocardiographic measurements, we thus studied 606 patients (533 men and 73 women) who had a myocardial infarction before the age of 60 years. The aldosterone synthase gene polymorphism was analyzed after polymerase chain reaction amplification and restriction enzyme digestion. The results demonstrated that there was no association of the aldosterone synthase gene polymorphism with echocardiographically determined left ventricular dimensions, wall thicknesses, or indexes of systolic or diastolic function. Furthermore, anthropometric data, including blood pressure levels, were balanced between the different genotypes. Finally, the allele frequency was similar for patients with myocardial infarction and a sample group from the normal population (n=1675). The data indicate that the allele status of the aldosterone synthase gene polymorphism is not useful for the identification of patients with myocardial infarction who have impaired left ventricular function or unfavorable remodeling.

Alleles↗
PubMed2000

Hormone replacement therapy and interrelation between serum interleukin-6 and body mass index in postmenopausal women: a population-based study.

Postmenopausal women are at increased risk to develop osteoporosis, coronary artery disease, heart failure, and hypertension. Interleukin-6 (IL-6) may be a pathogenetic element in these disorders. Serum IL-6 levels increase during aging and seem to be related to increased body fat mass. In the present retrospective study we aimed to investigate the role of hormone replacement therapy (HRT) on serum IL-6 levels and the interrelation of IL-6 and body fat mass. Parameters were assessed in a population-based sample of postmenopausal women (n = 302) and, for comparison, 245 men of the same age. Women with HRT (n = 92) had significantly lower serum IL-6 levels compared to subjects without HRT, which was independent of age, antihypertensive therapy, smoking habits, and blood pressure (1.5 +/- 0.1 vs. 2.9 +/- 0.6 pg/mL; P = 0.017). In women without HRT, the body mass index (BMI) was correlated with serum IL-6 levels (P < 0.001). Multivariate analysis controlling simultaneously for the effects of blood pressure and heart rate confirmed the positive correlation (P = 0.001). However, in subjects with HRT no such correlation between IL-6 and BMI was demonstrated, which was confirmed after controlling covariates. In male subjects, BMI correlated with serum IL-6 (P = 0.009), which was, however, blunted after controlling for blood pressure and heart rate, probably indicating an influence of the sympathetic nervous system on this interrelation. In conclusion, women receiving HRT display lower serum IL-6 levels and a blunted interrelation of IL-6 and BMI. As IL-6 may be a pathogenetic factor in age-related diseases, HRT-related inhibition of IL-6 secretion could be an important element for the favorable effects of HRT in postmenopausal women.

Aged↗
PubMed1999

Lack of association between a polymorphism of the aldosterone synthase gene and left ventricular structure.

BACKGROUND: Cardiac growth and function may be modulated in part by trophic effects of neurohormones. Specifically, aldosterone has been shown to stimulate the growth of cardiac myocytes and the accumulation of cardiac extracellular matrix proteins. Moreover, a variant of the aldosterone synthase gene (a cytosine/thymidine exchange at position -344 in the transcriptional regulatory region) has been associated with enlargement and disturbed filling of the left ventricle (LV) in a small sample of young white adults. The aim of the present study was to reinvestigate the implications of aldosterone synthase -344C/T allele status for serum aldosterone levels, blood pressure, and LV structure and function in large population-based samples. METHODS AND RESULTS: Individuals who participated in the echocardiographic substudy of the third MONICA (MONitoring trends and determinants in CArdiovascular disease) survey (n=1445) or in the second follow-up of the first MONICA survey (n=562) were studied by standardized anthropometric, echocardiographic, and biochemical measurements as well as genotyping for aldosterone synthase -344C/T allele status. In both surveys, the distribution of sex, age, arterial blood pressure, and body mass index was homogeneous in the aldosterone synthase genotype groups. Echocardiographic LV wall thicknesses, dimensions, and mass indexes were not significantly associated with a specific aldosterone synthase genotype. Likewise, no association was detectable with echocardiographic measures of LV systolic or diastolic function. Data were consistent in both samples and not materially different in subgroups defined by age, sex, or intake of antihypertensive medication. Finally, no significant association was observed for aldosterone synthase allele status and serum aldosterone levels in the group of 562 individuals. CONCLUSIONS: The data are not in favor of a significant contribution of the C/T exchange at position -344 in the aldosterone synthase transcriptional regulatory region to the variability of serum aldosterone levels, blood pressure, or cardiac size or function as found in 2 white population-based samples.

Adult↗
PubMed1999

Evidence for a vasopressin system in the rat heart.

Traditionally, a hypothalamo-neurohypophysial system is thought to be the exclusive source of arginine vasopressin (AVP), a potent antidiuretic, vasoconstricting, and growth-stimulating neuropeptide. We have identified de novo synthesis of AVP in the heart as well as release of the hormone into the cardiac effluents. Specifically, molecular cloning of sequence tags amplified from isolated, buffer-perfused, and pressure-overloaded rat hearts allowed the detection of cardiac AVP mRNA. Subsequent experiments revealed a prominent induction of AVP mRNA (peak at 120 minutes, 59-fold, P<0. 01 versus baseline) and peptide (peak at 120 minutes, 11-fold, P<0. 01 versus baseline) in these isolated hearts. Newly induced vasopressin peptide was localized most prominently to endothelial cells and vascular smooth muscle cells of arterioles and perivascular tissue using immunohistochemistry. In addition to pressure overload, nitric oxide (NO) participated in these alterations, because inhibition of NO synthase by Nomega-nitro-L-arginine methyl ester markedly depressed cardiac AVP mRNA and peptide induction. Immediate cardiac effects related to cardiac AVP induction in isolated, perfused, pressure-overloaded hearts appeared to be coronary vasoconstriction and impaired relaxation. These functional changes were observed in parallel with AVP induction and largely prevented by addition of a V1 receptor blocker (10(-8) mol/L [deamino-Pen1, O-Me-Tyr2, Arg8]-vasopressin) to the perfusion buffer. Even more interesting, pressure-overloaded, isolated hearts released the peptide into the coronary effluents, offering the potential for systemic actions of AVP from cardiac origin. We conclude that the heart, stressed by acute pressure overload or NO, expresses vasopressin in concentrations sufficient to cause local and potentially systemic effects.

Animals↗
PubMed1999

Risk predictors in patients scheduled for percutaneous coronary revascularization.

Traditionally, procedural risks associated with conventional balloon coronary angioplasty have been largely attributed to unfavorable lesion morphology. However, factors predicting adverse events in the current practice of percutaneous coronary revascularization are unclear. The present study was undertaken to determine factors predicting major adverse events (death or Q-wave myocardial infarction or emergency bypass surgery) in 3,335 consecutive patients undergoing percutaneous coronary revascularization in the current practice of percutaneous coronary revascularization. During the period of observation, the rate of lesions treated successfully increased from 91% to 95% (P < 0.0001), whereas the rate of major adverse events (MACE) decreased from 3.6% to 1.6% (odds ratio [OR], 0.70 per year). Using multiple stepwise logistic regression analysis, cardiogenic shock (OR, 8.59; confidence interval [CI], 4.27-17.27), renal disease (OR, 3.33; CI, 1.95-5.69), evolving myocardial infarction (OR, 2.80; CI, 1.47-5.31), congestive heart failure (OR, 2.18; CI, 1.23-3.86), total number of lesions treated (OR, 1.28; CI, 1.03-1.59), age (OR, 1.03; CI, 1.01-1.06), and history of prior coronary intervention (OR, 0.51; CI 0.26-0.99) were identified as independent predictors of MACE. In addition, vascular disease (OR, 2. 48; CI 1.37-4.50) and unstable angina pectoris (OR, 0.44; CI 0.25-0. 79) were related to adverse events when patients in cardiogenic shock were excluded from the model. With the exception of most unfavorable lesion morphology (AHA/ACC lesion type C; OR, 2.05; CI, 1.19-3.52), anatomic parameters added no further information. In the present era of device technology, success rates of percutaneous coronary revascularization procedures have increased and remain to be determined by lesion morphology. In contrast, the rate of MACE is declining and best predicted by easily identified patient characteristics.

Aged↗
PubMed1999

The cardiac endothelin system in established pressure overload left ventricular hypertrophy.

In normal hearts, endothelin-1 (ET-1) has been shown to initiate myocyte growth and to modulate cardiac function. However, regulation of the various components of the system and the functional effects of ET-1 in established left ventricular hypertrophy (LVH) are less clear. We thus studied ET-1, ET(A) receptor, and endothelin converting enzyme (ECE-1) mRNA regulation as well as the effects of ET-1 on coronary resistance, LV contractility and relaxation in hypertrophied rat hearts. Cardiac pressure overload, secondary to banding of the ascending aorta, resulted in a transient increase of cardiac ET-1 and ET(A) receptor mRNAs that reached a maximum at 2 days (+75% and +40%, respectively, P<0.05, each). ET-1 mRNA levels reached a second peak at 84 days of pressure overload (+60%, P<0.05), at the later time point in conjunction with elevated ECE-1 mRNA levels (+20%, P<0.05). The functional implications of ET-1 were examined in a study of isolated perfused hearts. Both hearts with established LVH and sham control hearts responded to ET-1 perfusion (10(-1)] to 10(-9) M) with an increase of coronary perfusion pressure (CPP; +85+/-15 and +75+/-8 mm Hg; P<0.001 each) and a slight decrease of LV systolic pressure (LVP; -12+/-9 and -9+/-7 mm Hg; P = NS). In contrast, ET-1 increased LV end-diastolic pressure (LVEDP) only in LVH hearts (+22+/-7 mm Hg, P<0.05 versus baseline and +20+/-7 mm Hg, P<0.05 versus sham). Direct stimulation of protein kinase C mimicked the effects of ET-1, whereas inhibition of this kinase or the Na+ -H+ exchanger blunted the effects of ET-1 on CPP, LVP, and LVEDP. Interestingly, coadministration of the vasodilator and the nitric oxide (NO) donor nitroglycerin not only prevented the increase of CPP and LVEDP, but also uncovered a slight positive inotropic effect of ET-1 in LVH hearts. Thus, the cardiac expression of ET-1, ET(A), and ECE-1 mRNAs displays a distinct pattern during early and advanced cardiac pressure overload. Furthermore, ET-1 mediates a slight depression of systolic, and a profound depression of diastolic, functional parameters in hearts with established LVH, effects that appear to be secondary to ET-1-related coronary vasoconstriction. The data suggest a functional role of the endothelin system in hearts with established pressure overload hypertrophy.

Amiloride↗
PubMed1999

Familial predisposition of left ventricular hypertrophy.

OBJECTIVES: The study evaluated the contribution of familial predisposition to the risk of left ventricular hypertrophy (LVH). BACKGROUND: Left ventricular hypertrophy is a multifactorial condition that serves as an important predictor of cardiovascular mortality. At present it is unclear whether familial predisposition contributes to the manifestation of LVH. Thus, we determined whether siblings of subjects with LVH are at increased risk to present with an elevation of LV mass or an abnormal LV geometry. METHODS: Echocardiographic and anthropometric measurements were performed in 2,293 individuals who participated in the echocardiographic substudies of population-based MONICA Augsburg surveys. In addition, a total of 319 siblings of survey participants with echocardiographic evidence of LVH were evaluated. The risk of these siblings to present with LVH or abnormal LV geometry was estimated by comparison with 636 subjects matched for gender and age that were selected from the entire echocardiography study base. RESULTS: Blood pressure, body mass index, age, and gender (i.e., known determinants of LV mass) were comparable in LVH-siblings and the matched comparison group. However, septal and posterior wall thicknesses, relative wall thickness as well as LV mass index were significantly elevated in LVH-siblings (p < 0.001, each) whereas LV dimensions did not differ. Likewise, the prevalence of LVH was raised in LVH-siblings, as was the relative risk of LVH after adjustment for confounders (p < 0.05). More specifically, LVH-siblings displayed increased prevalences of concentric remodeling and concentric LVH (p < 0.05) but not of eccentric LVH. CONCLUSIONS: Familial predisposition appears to contribute to increased LV wall thickness, to the development of LV hypertrophy and abnormal LV geometry.

Adult↗
PubMed1999

Implications of small reference vessel diameter in patients undergoing percutaneous coronary revascularization.

OBJECTIVES: The purpose of this study was to determine whether small reference diameter of the culprit coronary artery influences the outcome of an attempted percutaneous revascularization procedure in the current era of interventional cardiology. BACKGROUND: Although the interventional strategy is largely determined by the size of the culprit coronary artery, earlier quantitative studies have not shown a worse acute outcome for small reference vessel diameter (< or =2.5 mm). METHODS: A total of 2,306 patients undergoing percutaneous coronary revascularization was divided in groups with reference diameters < or =2.5 mm (n = 813) or >2.5 mm (n = 1,493). Success and in-hospital major adverse cardiac event (death, Q-wave myocardial infarction and emergency coronary artery bypass graft) rates between both groups were compared. RESULTS: Patients with lesions in small vessels were older and presented more frequently with female gender, diabetes mellitus, heart failure, peripheral vascular, multivessel coronary disease and American Heart Association/American College of Cardiology (AHA/ACC) lesion type C (p < or = 0.01, each). Further, utilization of interventional devices differed markedly. In contrast to stents (18.5% vs. 41.9%) and directional atherectomy (3.7% vs. 13.5%), conventional balloon angioplasty (73% vs. 50%) and rotational atherectomy (16.1% vs. 8.3%) were used more often in smaller vessels (p < or = 0.0001, each). Success rate was lower in the small vessel group (92% vs. 95%; p = 0.006). Major adverse cardiac events occurred more frequently in small than large vessels (univariate 3.4% vs. 2.0%, p = 0.03; multivariate odds ratio 2.1, p = 0.02), particularly when proximal coronary segments were compared. CONCLUSIONS: Lesions in vessels with small reference diameter represent a distinct group with respect to clinical and morphologic characteristics as well as device utilization. These lesions have lower chances of successful percutaneous intervention and carry relatively higher risks, specifically when located in proximal coronary segments.

Aged↗
PubMed1999

Central vasopressin is modulated by chronic blockade of the renin-angiotensin system in experimental left ventricular hypertrophy.

We studied the interaction of the central renin-angiotensin system (RAS) and vasopressin system in rats with left ventricular hypertrophy (LVH) due to aortic banding. In these animals plasma vasopressin is elevated and vasopressin content is increased in specific brain areas. Chronic blockade of the RAS by angiotensin-converting enzyme (ACE) inhibition (ramipril) and AT1 receptor antagonism (losartan) significantly attenuated circulating and central vasopressin in rats with LVH. Given the antidiuretic, vasoconstrictive, and growth-promoting effects, vasopressin may participate in the cardiovascular alterations in LVH. Blockade of the RAS strongly ameliorates central and peripheral-vasopressin. Therefore, central modulatory effects on vasopressin might contribute to the therapeutic efficacy of ACE inhibitors and AT1 antagonists.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Relation between dehydroepiandrosterone sulfate and blood pressure levels in a population-based sample.

Endogenous dehydroepiandrosterone sulfate (DHEAS) levels have been reported to be positively related to blood pressure levels. To further analyze this association, we quantified DHEAS in middle-aged subjects (mean age +/-SEM: 57.8+/-0.1 years) of a population-based sample (n = 646). DHEAS levels were higher in hypertensive as compared with normotensive individuals (1.26+/-0.04 v. 1.09+/-0.03 microg/mL, P = .01). After adjustment for age, gender, and body mass index, DHEAS levels were significantly related to systolic blood pressure (P = .01). In addition, in a subgroup of individuals without antihypertensive medication adjusted DHEAS levels were significantly related to systolic and diastolic blood pressure (n = 461; P<.05, both). DHEAS levels were also related to aldosterone (r = 0.15; P = .002) and androstenedione (its main metabolite; r = 0.66; P<.001) but not to renin levels. Like DHEAS, aldosterone, but not androstenedione, was significantly related to blood pressure levels and hypertension status. In a regression analysis that accounted for aldosterone and renin levels, both DHEAS and aldosterone kept their significant relationships with systolic blood pressure levels. Taken together, we observed a consistent positive association between endogenous DHEAS and systolic blood pressure levels that was independent of other, similarly regulated, adrenal steroids.

Aged↗
PubMed1999

Association of arginine vasopressin and arterial blood pressure in a population-based sample.

BACKGROUND: The role of arginine vasopressin (AVP) in the development and maintenance of arterial hypertension is controversial. Furthermore, it remains unclear whether chronic treatment with antihypertensive agents modulates levels of AVP, with potential secondary effects on vascular tone and fluid homeostasis. OBJECTIVE: To investigate the relation between plasma AVP and arterial blood pressure in a population-based sample of 534 middle-aged subjects. RESULTS: Overall, levels of AVP were higher in hypertensive subjects (2.15 +/- 0.26 pg/ml; n = 289) than in normotensive subjects (1.45 +/- 0.15 pg/ml; n = 245; P < 0.05). (Hypertension was defined as systolic blood pressure > 160 mmHg and/or diastolic blood pressure > 95 mmHg, or receiving antihypertensive medication.) In untreated individuals, plasma levels of AVP were found to be correlated with both systolic (r = 0.15, P = 0.002) and diastolic (r = 0.14, P = 0.005) blood pressure. The differences between the lowest and highest quartile of AVP levels were 5.1 mmHg (P = 0.03) and 2.6 mmHg (NS) for systolic and diastolic blood pressure, respectively, after adjustment for age and sex. Moreover, it appeared that the relation between AVP and blood pressure was particularly strong in subjects with low levels of renin (< 10 mU/l; n = 118; systolic blood pressure r = 0.24, P = 0.007; diastolic blood pressure r = 0.19, P = 0.03). Specifically, patients receiving monotherapy with diuretics (n = 39) or beta-blockers (n = 54) displayed elevated plasma levels of AVP (2.93 +/- 0.98 pg/ml and 2.74 +/- 0.74 pg/ml respectively); however, only in patients taking diuretics was this finding apparently independent of confounding variables. Other monotherapies with angiotensin-converting enzyme inhibitors (n = 9) or Ca(2+)-antagonists (n = 19) were not associated with levels of AVP. CONCLUSION: The data suggest that plasma levels of AVP display a discernible relationship with arterial blood pressure and hypertension, particularly when renin levels are low. In addition, with the exception of diuretics, no modulation of AVP levels is attributable to the intake of antihypertensive agents as it occurs in a population-based sample.

Aged↗
PubMed1998

Changes in left ventricular structure and function in patients with white coat hypertension: cross sectional survey.

OBJECTIVES: To assess the relation between white coat hypertension and alterations of left ventricular structure and function. DESIGN: Cross sectional survey. SETTING: Augsburg, Germany. SUBJECTS: 1677 subjects, aged 25 to 74 years, who participated in an echocardiographic substudy of the monitoring of trends and determinants in cardiovascular disease Augsburg study during 1994-5. OUTCOME MEASURES: Blood pressure measurements and M mode, two dimensional, and Doppler echocardiography. After at least 30 minutes' rest blood pressure was measured three times by a technician, and once by a physician after echocardiography. Subjects were classified as normotensive (technician <140/90 mm Hg, physician <160/95 mm Hg; n=849), white coat hypertensive (technician <140/90 mm Hg, physician >=160/95 mm Hg; n=160), mildly hypertensive (technician >=140/90 mm Hg, physician <160/95 mm Hg; n=129), and sustained hypertensive (taking antihypertensive drugs or blood pressure measured by a technician >=140/90 mm Hg, and physician >=160/95 mm Hg; n=538). RESULTS: White coat hypertension was more common in men than women (10.9% versus 8.2% respectively) and positively related to age and body mass index. After adjustment for these variables, white coat hypertension was associated with an increase in left ventricular mass and an increased prevalence of left ventricular hypertrophy (odds ratio 1.9, 95% confidence interval 1.2 to 3.2; P=0.009) compared with normotensive patients. The increase in left ventricular mass was secondary to significantly increased septal and posterior wall thicknesses whereas end diastolic diameters were similar in both groups with white coat hypertension or normotension. Additionally, the systolic white coat effect (difference between blood pressures recorded by a technician and physician) was associated with increased left ventricular mass and increased prevalence of left ventricular hypertrophy (P<0.05 each). Values for systolic left ventricular function (M mode fractional shortening) were above normal in subjects with white coat hypertension whereas diastolic filling and left atrial size were similar to those in normotension. CONCLUSION: About 10% of the general population show exaggerated inotropic and blood pressure responses when mildly stressed. This is associated with an increased risk of left ventricular hypertrophy.

Adult↗
PubMed1998

[A case of Carney complex].

HISTORY AND CLINICAL FINDINGS: For some months a 57-year-old woman had noted increasing shortness of breath, associated in the last few weeks with undirected vertigo and several brief periods of lost consciousness. She was finally admitted because of additional central facial paresis. On auscultation a high-frequency systolic murmur was heard over the apex and a discrete diastolic murmur over Erb's point. There were numerous facial freckles and three cutaneous myxomas. INVESTIGATIONS: Echocardiography revealed irregular tumours throughout the left atrium and a large broad-based one prolapsing through the mitrale valve in diastole. Computed tomography demonstrated a 6 x 6 cm tumour in the left lower abdomen, probably arising from the left ovary, and a second 3 x 3 cm presacral tumour. TREATMENT AND COURSE: At cardiac surgery four tumours were found in the left atrium and resected: histologically they were benign myxomas. Removal required extensive resection in the area of the interatrial septum and the atrial wall, resulting in 2 degrees AV block for which a VDD pacemaker was implanted. CONCLUSION: Atrial myxomas may be the cardinal sign of the Carney Complex, an autosomal dominant syndrome with cutaneous myxomas, myxoid abdominal tumours, hormone-producing tumours in the testicles, adrenal cortex or hypophysis, schwannoma as well as lentigines. For this reason, further tumours should be looked for if freckles and/or cutaneous tumours are found in association with an atrial myxoma. The patient and family should be informed about the genetic aspects.

Dyspnea↗