An impairment of glucose metabolism, contributing to the increased cardiovascular risk, has been shown in primary aldosteronism (PA). Insulin resistance is associated with nonalcoholic fatty liver disease (NAFLD) and may play a role in its pathophysiology. The aim of this study was to investigate the association between NAFLD and PA, and to identify determinants of NAFLD in this condition.A total of 40 patients with PA, 40 sex-, age-, and body mass index matched patients with low-renin essential hypertension (LREH) and 40 normotensive subjects were studied. According to ultrasound detection of fatty liver, each group was subdivided in two subsets: with NAFLD and without NAFLD. Patients with diabetes, obesity, and hyperlipidemia were excluded.Prevalence of NAFLD in PA was similar to that observed in LREH patients, and higher (P < 0.01) than in normotensive controls. Serum potassium was lower in PA than in LREH patients with NAFLD (P < 0.001), while it was similar in PA and LREH patients without NAFLD. At univariate analysis, plasma aldosterone, homeostasis model assessment (HOMA) index and hypokalemia were determinants of NAFLD in PA (P < 0.05), while HOMA index was associated with NAFLD in LREH (P < 0.05). At multivariable analysis, only hypokalemia remained associated with NAFLD in PA (P = 0.02).The results of this pilot study suggest that, in the absence of major risk factors for liver disease, NAFLD is a frequent finding in PA. Patients with PA and hypokalemia are more insulin resistant and have higher prevalence of NAFLD than those with normokalemia, indicating greater risk for metabolic and liver disease in this subgroup.
Objective: The aim of this study is to evaluate the cause of CFR impairment in DCM patients by correlating functional CFR assessed and microvascular structural abnormalities measured on endomyocardial biopsy (EMB). Materials and methods: We evaluated EMBs from 26 consecutive DCM patients and EMBs from 11 consecutive Heart Transplant patients. We performed morphometric analysis on EMBs. We measured myocyte mean diameter, capillary density, microvascular remodeling (vessel media area/total vessel area ratio (%)). Coronary flow velocity in the left anterior descending coronary artery was detected by Transthoracic Doppler Echocardiography (TDE) at rest and during adenosine infusion. CFR was the ratio of hyperemic diastolic flow velocity (DFV) to resting DFV. A CFR≤2.5 was considered abnormal. The results were compared to a control group, consisted of 11 heart-transplant (HTx) patients with impaired CFR due to microvascular remodeling. Results: Despite CFR in DCM patients is comparable to the HTx pts (2,25±0,61 vs. 2,0±0,5, p=0.4), microvascular remodeling is significantly lower in DCM pts compared to HTx group (43,93±7,12% vs. 72,3±8,0%, p<0,0001). In DCM patients capillary density (194,83±22,63 vs. 157,2±42,4, p=0,03), fibrosis (19,44±7,55% vs. 6,8±5,0%, p<0,02) and myocyte mean diameter (23,79±3,01μm vs. 20,5±3,7μm, p=0,5) are significantly higher than in HTx group. In DCM patients CFR shows a significant inverse correlation with central venous pressure (r= -0,692, p=0,02), with right heart pressure (r= -0,609, p=0,05) and with NTproBNP (r= -0,754, p=0,01) and a positive correlation with cardiac output (r=0,737, p=0,01) and oxygen consumption (r=0,412, p=0,02). Conclusion: CFR impairment in DCM patients is not related to microvascular remodeling. It is closely related to cardiac performance and the patient's clinical status. Patients with pathological CFR (CFR<2,5) have a poorer prognosis, since they have worsen clinical and hemodynamic conditions.
Symptomatic primary hyperparathyroidism (PHPT) is associated with increased cardiovascular mortality. However, data on the association between asymptomatic PHPT and cardiovascular risk are lacking. We assessed coronary flow reserve (CFR) as a marker of coronary microvascular function in asymptomatic PHPT of recent onset.We studied 100 PHPT patients (80 women; age, 58±12 years) without cardiovascular disease and 50 control subjects matched for age and sex. CFR in the left anterior descending coronary artery was detected by transthoracic Doppler echocardiography, at rest, and during adenosine infusion. CFR was the ratio of hyperemic to resting diastolic flow velocity. CFR was lower in PHPT patients than in control subjects (3.0±0.8 versus 3.8±0.7; P<0.0001) and was abnormal (≤2.5) in 27 patients (27%) compared with control subjects (4%; P=0.0008). CFR was inversely related to parathyroid hormone (PTH) levels (r=-0.3, P<0.004). In patients with CFR ≤2.5, PTH was higher (26.4 pmol/L [quartiles 1 and 3, 16 and 37 pmol/L] versus 18 [13-25] pmol/L; P<0.007), whereas calcium levels were similar (2.9±0.1 versus 2.8±0.3 mmol/L; P=0.2). In multivariable linear regression analysis, PTH, age, and heart rate were the only factors associated with CFR (P=0.04, P=0.01, and P=0.006, respectively). In multiple logistic regression analysis, only PTH increased the probability of CFR ≤2.5 (P=0.03). In all PHPT patients with CFR ≤2.5, parathyroidectomy normalized CFR (3.3±0.7 versus 2.1±0.5; P<0.0001).PHPT patients have coronary microvascular dysfunction that is completely restored after parathyroidectomy. PTH independently correlates with the coronary microvascular impairment, suggesting a crucial role of the hormone in explaining the increased cardiovascular risk in PHPT.
Background:Psoriasis (Ps) is a recently recognized independent determinant for myocardial infarction (MI), associated with cardiovascular risk factors.We investigated whether coronary flow reserve (CFR), an index of coronary microvascular function, was impaired in young patients with Ps and the relationship between clinical markers of Ps activity and coronary blood flow abnormalities. Methods: 56 patients (pts) with Ps (42 M, aged 37±7 years) without clinical evidence of heart diseases, and 48 controls matched for age and sex were studied. Coronary flow velocity in the left anterior descending coronary artery was detected by transthoracic Doppler echocardiography at rest and during adenosine infusion. CFR was the ratio of hyperaemic diastolic flow velocity (DFV) to resting DFV. A CFR ≤2.5 was considered abnormal. Mean time from diagnosis of Ps was 17±7 years. Results: In pts with Ps, CFR was lower than in controls (3.2±0.9 vs 3.7±0.7, p=0.02). CFR was abnormal (≤2.5) in 12 pts with Ps (22% vs 0% controls,...
Abstract Aims Clinical case—Twenty-four years old Moroccan woman. Family history: parents and three siblings in good health. Methods and results Past medical history—In 2016, when she was 19 years old, she developed worsening exercise-induced dyspnoea. A right heart catheterization (RHC) was performed with evidence of increased median pulmonary artery pressure (mPAP 60 mmHg, wedge pressure 8 mmHg), cardiac index 2.27 l/min/m2. She was diagnosed with idiopathic pulmonary hypertension and combination therapy with sildenafil and macitentan was started with partial improvement. In August 2019, she became pregnant and vasodilatory therapy was suspended. The pregnancy was complicated by premature labor with foetal death. Specific therapy with sildenafil and macitentan was then restarted. Due to further clinical and haemodynamic impairment, triple combination therapy with selexipag was initiated. However, symptomatic deterioration progressed, and she was referred to a Pulmonary Hypertension Referral Center where HRTC of the chest showed centrilobular ground-glass opacities and interlobular septal thickening. Based on the imaging that was highly suspicious pulmonary veno-occlusive disease (PVOD), and the severe haemodynamic impairment (with pulmonary vascular resistance at RHC > 20 WU), assessment for lung transplantation was started. Recent medical history—she was transferred to our Center with Transplant Unit for lung transplant assessment. Pulmonary function testing demonstrated a restrictive disorder with severe reduction of DLCO (14%). At 6-min walking test, she could walk 100 m with desaturation up to 90% on O2 therapy. Evaluated by our multidisciplinary team, indications for lung transplantation were confirmed and she entered the transplant waiting list. At the end of February 2021: further clinical and haemodynamic deterioration with respiratory distress, reduction in urinary output and signs and symptoms of right-side heart failure; she was hospitalized in intensive care unit and required extra-corporeal membrane oxygenation (ECMO) circulatory support. Selexipag was suspended. On echocardiography: severe right ventricle hypertrophy and dilatation, tricuspid regurgitation velocity >4 m/s. Few days later, she underwent bilateral lung transplantation; anatomo-pathological evaluation of explanted organs confirmed PVOD. However, during post-operative monitoring, she suffered from two episodes of cardiac arrest on VT/VF which required multiple DC-shocks. Since no triggering causes were identified, an ICD was implanted for secondary prevention. Conclusions PVOD is a rare disease with clinical presentation and haemodynamic profile often similar to pulmonary arterial hypertension (and, therefore, the diagnosis is challenging) but the clinical course is more severe. The diagnosis requires clinical history and physical examination, together with multimodality imaging and functional testing. Bronchoalveolar lavage might be necessary. Patients do not usually respond satisfactorily to vasodilatory therapy but rather they are at high risk of drug-induced pulmonary oedema. Some case reports and case series have reported a slight benefit and/or clinical stabilization with vasodilatory therapy in selected patients; therefore, specific therapy can be used but cautiously and in experienced referral centres. Definitive therapy is lung transplantation (or heart-lung transplantation) and a multidisciplinary team is necessary for the appropriate management of these complicated patients. Ventricular arrhythmias are rare in patients with Group 1 pulmonary hypertension. In our specific clinical case, we suspect that ventricular arrhythmias might be related to the severely hypertrophic, and potentially fibrotic, right ventricle.
