Office blood pressure threshold of 130/80 mmHg better predicts uncontrolled out-of-office blood pressure in apparent treatment-resistant hypertension.

The objective of this study was to compare the diagnostic accuracy of office blood pressure (BP) threshold of 140/90 and 130/80 mmHg for correctly identifying uncontrolled out-of-office BP in apparent treatment-resistant hypertension (aTRH). We analyzed 468 subjects from a prospectively enrolled cohort of patients with resistant hypertension in South Korea (clinicaltrials.gov: NCT03540992). Resistant hypertension was defined as office BP ≥ 130/80 mmHg with three different classes of antihypertensive medications including thiazide-type/like diuretics, or treated hypertension with four or more different classes of antihypertensive medications. We conducted different types of BP measurements including office BP, automated office BP (AOBP), home BP, and ambulatory BP. We defined uncontrolled out-of-office BP as daytime BP ≥ 135/85 mmHg and/or home BP ≥ 135/85 mmHg. Among subjects with office BP < 140/90 mmHg and subjects with office BP < 130/80 mmHg, 66% and 55% had uncontrolled out-of-office BP, respectively. The prevalence of controlled and masked uncontrolled hypertension was lower, and the prevalence of white-coat and sustained uncontrolled hypertension was higher, with a threshold of 130/80 mmHg than of 140/90 mmHg, for both office BP and AOBP. The office BP threshold of 130/80 mmHg was better able to diagnose uncontrolled out-of-office BP than 140/90 mmHg, and the net reclassification improvement (NRI) was 0.255. The AOBP threshold of 130/80 mmHg also revealed better diagnostic accuracy than 140/90 mmHg, with NRI of 0.543. The office BP threshold of 130/80 mmHg showed better than 140/90 mmHg in terms of the correspondence to out-of-office BP in subjects with aTRH.

Relationship between the ST-Segment Resolution and Microvascular Dysfunction in Patients Who Underwent Primary Percutaneous Coronary Intervention.

OBJECTIVES: Incomplete ST-segment elevation resolution (STR) occasionally occurs despite successful revascularization of epicardial coronary artery after primary percutaneous coronary intervention (PPCI). The aim of this study was to evaluate the relationship between the degree of STR and the severity of microvascular dysfunction. METHODS: A total of 73 consecutive patients with ST-segment elevation myocardial infarction (STEMI) who underwent successful PPCI were evaluated. Serial 12-lead electrocardiography was performed at baseline and at 90 minutes after PPCI. Microvascular dysfunction was assessed by index of microvascular resistance (IMR) immediately after PPCI. RESULTS: Patients were classified into 2 groups: 50 patients with complete STR (STR ≥50%) and 23 patients with incomplete STR (STR <50%). The incomplete STR group had a higher IMR value and lower left ventricular ejection fraction (LVEF), compared with the complete STR group. The degree of STR was significantly correlated with IMR (r = -0.416, P=0.002) and LVEF (r = 0.300, P=0.011). These correlations were only observed in patients with left anterior descending artery (LAD) infarction but not observed in patients with non-LAD infarction. A cutoff IMR value was 27.3 for predicting incomplete STR after PPCI. CONCLUSION: Incomplete STR after PPCI in patients with STEMI reflects the presence of microvascular and left ventricular dysfunction, especially in patients with LAD infarction.

Kallmann syndrome with a Tyr113His PROKR2 mutation.

RATIONAL: Kallmann syndrome (KS) is a genetic gonadotropin-releasing hormone deficiency associated with hyposmia or anosmia and characterized by various modes of inheritance. PATIENT CONCERNS: A 16-year-old male did not reach puberty and was associated with hypogonadotropic hypogonadism and anosmia. His magnetic resonance imaging of brain revealed the absence of the olfactory bulb. DIAGNOSIS: His karyotype was 46 XY. Sanger sequencing of the KAL1 gene revealed no mutations. Diagnostic exome sequencing identified a prokineticin-receptor 2 (PROKR2) gene variant, c.337T > C (p.Tyr113His), previously reported to be a pathogenic mutation; we confirmed the presence of the mutation via Sanger sequencing of the coding exons of PROKR2. His apparently unaffected mother and sister, but not his father, were heterozygous for the PROKR2 Tyr113His mutation. LESSONS: This work advances our understanding of the role played by PROKR signaling and the mode of inheritance of the gene in patients with KS.