Lipid-Lowering Therapy after Acute Coronary Syndrome in Outpatient Practice-How to Achieve Goal.

BACKGROUND: Secondary prevention of cardiovascular disease involves the use of optimal pharmacological treatment and modification of risk factors through lifestyle changes. Recent evidence demonstrates that the major initiating event in atherogenesis is the storage of low-density lipoproteins. OBJECTIVES: We aimed to compare the efficacy in achieving the therapeutic lipid target in relation to the frequency of follow-up at selected time points and to determine the safety and tolerability of cholesterol-lowering drugs (statins, ezetimibe). METHODS: This was a prospective analysis of 72 consecutive patients hospitalized for acute coronary syndrome: ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). Patients were consecutively divided into two groups: first, with follow-up and laboratory tests at 1, 3, 6 and 12 months after hospital discharge, including 32 patients; second, including 40 patients with follow-up and laboratory tests 12 months after hospital discharge. RESULTS: A significant reduction in LDL-C level was observed at 12 months in both groups. LDL-C level was significantly lower in group 1 than in group 2 after 12 months (p = 0.02). Total cholesterol level was significantly lower in group 1 than in group 2 after 12 months. After 12 months of therapy, 21 (65.6%) patients in group 1 and 17 (42.5%) in group 2 had LDL-C < 1.4 mmol/L. In group 1, we observed a significant decrease in LDL-C, triglyceride, and total cholesterol levels at 1, 3, 6 and 12 months (p < 0.05). CONCLUSIONS: The group of patients with more frequent follow-up visits showed a greater reduction in LDL-C level than the group with only one visit after a 12-month hospital discharge.

Anatomic Variations of Renal Arteries as an Important Factor in the Effectiveness of Renal Denervation in Resistant Hypertension.

Hypertension remains the leading cause of death worldwide. Despite advances in drug-based treatment, many patients do not achieve target blood pressure. In recent years, there has been an increased interest in invasive hypertension treatment methods. Long-term effects and factors affecting renal denervation effectiveness are still under investigation. Some investigators found that the renal arteries' morphology is crucial in renal denervation effectiveness. Accessory renal arteries occur in 20-30% of the population and even more frequently in patients with resistant hypertension. Diversity in renal vascularization and innervation may complicate the renal denervation procedure and increase the number of people who will not benefit from treatment. Based on previous studies, it has been shown that the presence of accessory renal arteries, and in particular, the lack of their complete denervation, reduces the procedure's effectiveness. The following review presents the anatomical assessment of the renal arteries, emphasizing the importance of imaging tests. Examples of imaging and denervation methods to optimize the procedure are presented. The development of new-generation catheters and the advancement in knowledge of renal arteries anatomy may improve the effectiveness of treatment and reduce the number of patients who do not respond to treatment.

Mavacamten - a new disease-specific option for pharmacological treatment of symptomatic patients with hypertrophic cardiomyopathy.

Current pharmacotherapy for hypertrophic cardiomyopathy (HCM) is not disease-specific and has suboptimal efficacy, often necessitating interventional treatment. EXPLORER-HCM was a phase 3, randomized, double-blind, placebo-controlled, multicenter clinical trial investigating the effects of mavacamten, a first-in-class selective cardiac myosin inhibitor, in patients with HCM, left ventricular outflow tract obstruction (LVOTO) and New York Heart Association (NYHA) class II or III symptoms. The primary endpoint was defined as either a ≥1.5 ml/kg/min increase in peak oxygen consumption (pVO2) and ≥1 NYHA class reduction or a ≥3.0 ml/kg/min pVO2 increase without NYHA class worsening. Secondary endpoints evaluated changes in post-exercise LVOT gradient, pVO2, NYHA class, Kansas City Cardiomyopathy Questionnaire-Clinical Summary Score (KCCQ-CSS), and Hypertrophic Cardiomyopa-thy Symptom Questionnaire Shortness-of-Breath subscore (HCMSQ-SoB). A total of 251 patients were randomized to receiving mavacamten or placebo. The primary endpoint and all secondary endpoints were met significantly more frequently in the mavacamten arm versus placebo. The safety profile of mavacamten was similar to that of placebo. In conclusion, disease-specific treatment with mavacamten in patients with obstructive HCM led to reduced LVOTO and improvement in both objective functional parameters and patient-related health status.

Reversed Septal Curvature Is Associated with Elevated Troponin Level in Hypertrophic Cardiomyopathy.

The aim of study was to compare patients with hypertrophic cardiomyopathy divided according to septal configuration assessed in a 4-chamber apical window. The study group consisted of 56 consecutive patients. Reversed septal curvature (RSC) and non-RSC were diagnosed in 17 (30.4%) and 39 (69.6%) patients, respectively. Both RSC and non-RSC groups were compared in terms of the level of high-sensitivity troponin I (hs-TnI), NT-proBNP (absolute value), NT-proBNP/ULN (value normalized for sex and age), and echocardiographic parameters, including left ventricular outflow tract gradient (LVOTG). A higher level of hs-TnI was observed in RSC patients as compared to the non-RSC group (102 (29.2-214.7) vs. 8.7 (5.3-18) (ng/l), p = 0.001). A trend toward increased NT-proBNP value was reported in RSC patients (1279 (367.3-1186) vs. 551.7 (273-969) (pg/ml), p = 0.056). However, no difference in the NT-proBNP/ULN level between both groups was observed. Provocable LVOTG was higher in RSC as compared to non-RSC patients (51 (9.5-105) vs. 13.6 (7.5-31) (mmHg), p = 0.04). Furthermore, more patients with RSC had prognostically unfavourable increased septal thickness to left LV diameter at the end diastole ratio. Patients with RSC were associated with an increased level of hs-TnI, and the only trend observed in this group was for the higher NT-proBNP levels. RSC seems to be an alerting factor for the risk of ischemic events. Not resting but only provocable LVOTG was higher in RSC as compared to non-RSC patients.

Serum N-terminal pro-B-type natriuretic peptide levels are associated with left atrial dilation, resting left ventricular outflow tract gradient, and pulmonary hypertension in patients with hypertrophic cardiomyopathy.

INTRODUCTION: N-terminal pro-B-type natriuretic peptide (NT-proBNP) can be a marker of left ventricle (LV) pressure overload in hypertrophic cardiomyopathy (HCM). The different clinical characteristics of HCM might correspond to the degree of NT-proBNP increase. AIM: This study aimed to establish whether the left atrium (LA) dimension, left ventricle outflow tract (LVOT) gradient, and pulmonary hypertension influence NT-proBNP serum levels in patients with HCM. MATERIAL AND METHODS: In 62 HCM patients (32 males and 30 females, mean age 31 ±11 years), echocardiography with LV outflow tract gradient provocation was performed using natural stimuli > 30 mm Hg (NOHCM - 36 patients, POHCM - 12 patients, HOCM - 14 patients). RESULTS: Smaller LAD was associated with a lower NT-proBNP/ULN level (p = 0.001). In contrast, smaller vs. larger LAD subgroups did not differ in NT-proBNP level (p = 0.42). Both NT-proBNP/ULN and NTproBNP were significantly elevated in the subgroup with lager LAA. The absolute value of NT-proBNP was significantly higher in the HOCM subgroup (NOHCM vs. POHCM vs. HOCM (p = 0.02). Similarly, NT-proBNP/ULN was significantly higher in the HOCM subgroup (NOHCM vs. POHCM vs. HOCM, p = 0.00047). This elevated value of biomarker is related to pulmonary hypertension. CONCLUSIONS: Increased NT-proBNP/ULN is positively associated with larger LAD and LAA, while elevated NTproBNP is only associated with larger LAA. The highest levels of both NT-proBNP and NTproBNP/ULN were associated with HOCM and pulmonary hypertension, whereas biomarker levels were comparably lower in both the POHCM and NOHCM.

Identification of a variant hotspot in MYBPC3 and of a novel CSRP3 autosomal recessive alteration in a cohort of Polish patients with hypertrophic cardiomyopathy.

INTRODUCTION: Hypertrophic cardiomyopathy (HCM) is a heart disorder caused by autosomal dominant alterations affecting both sarcomeric genes and other nonsarcomeric loci in a minority of cases. However, in some patients, the occurrence of the causal pathogenic variant or variants in homozygosity, compound heterozygosity, or double heterozygosity has also been described. Most of the HCM pathogenic variants are missense and unique, but truncating mutations of the MYBPC3 gene have been reported as founder pathogenic variants in populations from Finland, France, Japan, Iceland, Italy, and the Netherlands. OBJECTIVES: This study aimed to assess the genetic background of HCM in a cohort of Polish patients. PATIENTS AND METHODS: Twenty­nine Polish patients were analyzed by a next generation sequencing panel including 404 cardiovascular genes. RESULTS: Pathogenic variants were found in 41% of the patients, with ultra­ rare MYBPC3 c.2541C>G (p.Tyr847Ter) mutation standing for a variant hotspot and correlating with a lower age at HCM diagnosis. Among the nonsarcomeric genes, the CSRP3 mutation was found in a single case carrying the novel c.364C>T (p.Arg122Ter) variant in homozygosity. With this finding, the total number of known HCM cases with human CSRP3 knockout cases has reached 3. CONCLUSIONS: This report expands the mutational spectrum and the inheritance pattern of HCM.

Predictors of syncope in patients with severe aortic stenosis: The role of orthostatic unload test.

BACKGROUND: There is a paucity of data regarding response of cerebral blood flow to the postural unloading maneuver and its impact on the risk of syncope in patients with aortic stenosis (AS). The aim of the present study was to assess effects of orthostatic stress test on changes in carotid and vertebral artery blood flow and its association with syncope in patients with severe AS. METHODS: 108 patients were enrolled (72 with and 36 patients without syncope) with severe isolated severe AS. Peak systolic blood-flow velocity (PSV) and end-diastolic velocity in the carotid arteries and vertebral arteries were measured by duplex ultrasound in the supine position and at 1-2 min after the assumption of the standing position. RESULTS: The orthostatic stress test induced a significant decrease in carotid and vertebral arterial flow velocities in all examined arteries (p < 0.001). The median (interquartile range) of mean change in PSV for carotid arteries was higher for patients with syncope (syncope [-] vs. syncope [+]: -0.6 cm/s [-1.8, 1.0] vs. -7.3 cm/s [-9.5, -2.0]; p < 0.001) and similarly for vertebral arteries (-0.5 cm/s [-2.0, 0.5] vs. -4.8 cm/s [-6.5, -1.3]; p < 0.001, respectively). Age, aortic valve area, and mean change in PSV for carotid arteries were independently associated with syncope. CONCLUSIONS: In patients with AS, a decrease in carotid and vertebral arterial flow velocities in the standing position was observed and was associated with syncope. The present findings may support the value of an orthostatic test in identifying patients with severe AS and a high risk of syncope.

Hypertrophic Cardiomyopathy: The Time-Synchronized Relationship between Ischemia and Left Ventricular Dysfunction Assessed by Highly Sensitive Troponin I and NT-proBNP.

The aim of this study was to compare NT-proBNP using the absolute values and NT-proBNP/ULN values that were standardized by age and gender between three subgroups: those without ischemia (negative hs-troponin I and no anginal pain (hsTnI-/AP-)), those with painless ischemia (hsTnI+/AP-), and those with painful ischemia (hsTnI+/AP+). Additionally, echocardiographic parameters were compared in these three subgroups. The absolute value of NT-proBNP was significantly higher in the painful ischemia subgroup (hsTnI-/AP- vs. hsTnI+/AP- vs. hsTnI+/AP+: 502 (174-833) vs. 969 (363-1346) vs. 2053 (323-3283) pg/ml; p = 0.018 for the whole-model analysis). The standardized value of NT-proBNP/ULN was gradually increased (hsTnI-/AP- vs. hsTnI+/AP- vs. hsTnI+/AP+: 3.61 + 0.63 vs. 6.90 + 1.31 vs. 9.35 + 1.87; p = 0.001 for the whole-model analysis). In the comparison between subgroups (hsTnI-/AP- vs. hsTnI+/AP- vs. hsTnI+/AP+), two echocardiographic parameters increased significantly. The left ventricular maximum wall thickness (LVMWT) at diastole was 1.99 ± 0.08 cm vs. 2.28 ± 0.13 cm vs. 2.49 ± 0.15 cm (p = 0.004 for the whole-model analysis). The maximal gradient of the provoked left ventricular outflow tract (LVOT) gradient increased significantly in only the painful-ischemia subgroup (11 (7-30) mmHg vs. 12 (9.35-31.5) mmHg vs. 100 (43-120) mmHg). In conclusion, both painless ischemia and painful ischemia are associated with a gradual, significant increase in NT-proBNP/ULN in comparison to the double-negative hsTnI/AP subgroup. In contrast, NT-proBNP is significantly higher in only the subgroup with painful ischemia.