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This is the tale in first person of how I discovered the “Tensive target organ damage/Monitoring prehypertension syndrome”, which received an acknowledgement of paternity with the nosographic eponym of “Cugini’s syndrome”. The presentation is made with the intention of showing how the research methodology and clinical reasoning can act as an epistemological guide, primarily in detecting and, secondarily in defining such a syndromic picture. I will narrate, in an anecdotal way, the history of this syndrome that has origin in 1980 when I received the invitation to approach, as Visiting Professor, the Chronobiology Laboratories of Minnesota University, directly from their legendary Chief, Prof. Franz Halberg, the Founder of the discipline “Chronobiology”. As an invited participant to an international project of research named: “International Womb-to-Tomb Chronome Initiative”, devoted to standardize the time-qualified reference limits of blood pressure from neonatal to old age, I could use the first available equipments (Pressurometers) for executing the Ambulatory Blood Pressure Monitoring. Accordingly, I started to collect the ABPM of a large sample size of clinically healthy subjects. Collection continued going back and forth between Italy and USA. In this activity of recruitment for creating a database of true normotensives and true hypertensives, I had the chance to meet some office normotensives who inexplicably showed initial signs of hypertensive retinopathy, a sign of “Target Organ Damage” (TOD), while, unexpectedly, were showing no supranormal BP values at the ABPM. In order to explain the retinal TOD, I suspected that they were true non-hypertensives but not true normotensives (presumably normotensives alias putative normotensives). Therefore, I compared the Daily Mean Level of their 24-h systolic (S) and diastolic (D) BP values [DML(SBP/DBP)] with the analogous estimate of the true normotensives. With surprise I could see that the retinopathic putative normotensives, despite the lack of surpranormal at the ABPM, had their DML(SBP/DBP) significantly increased, just in between true normotension and true hypertension. It was the year 1997, when I called this intermediate BP regimen: “ABPM-diagnosable prehypertension”, alias “monitoring prehypertension”, alias “pressurometric prehypertension”, alias “masked prehypertension”, and described the “Minimal-change hypertensive retinopathy/monitoring prehypertension syn- drome”. The association of a minimal tensive TOD with a monitoring prehypertension in office normotensives received a confirmatory certainty in other consecutive investigations, performed by me from 1997 to 2002, dealing with minimal signs respectively of: 1. interventricular septum hypertrophy in native hearts, 2. interventricular septum hypertrophy in novel transplanted hearts, 3. gestational impaired blood flow uterine arteries, 4. intrauterine growth retardation, 5. endothelial dysfunction. In all these clinical pictures, I could demonstrate that the initial tensive TOD was associated to a significant elevation of DML(SBP/DBP) just in between normotension and hypertension as per a monitoring prehypertension. Accordingly, I enlarged the appellative of the syndromic picture in “Minimal signs of TOD/monitoring prehypertension”, alias “Tensive target organ damage/Monitoring prehypertension”. Importantly, in 2007 and 2009 this clinical association has been eponimically called: “Cugini’s syndrome” in an international context.
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