The complications of T2DM are conventionally divided into microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (coronary heart disease, cerebrovascular disease, peripheral artery disease, heart failure). The division is convenient and dangerous. Convenient, because the screening calendars and the evidence base for interventions differ. Dangerous, because the student starts to think: first "small vessels", then "large ones", and a macrovascular catastrophe comes "late". A person with newly diagnosed T2DM may already have a myocardial infarction in their history while the fundus is still "clean". This is not a paradox but different mechanisms living on a common background of resistance, hyperglycaemia, hypertension and dyslipidaemia.
The microvascular series is most closely linked to the duration and degree of hyperglycaemia. Opening Section 12, ADA 2026 names chronic hyperglycaemia as the most established contributing factor to microvascular complications. The proof of the effect of glycaemic control on small vessels in T2DM is UKPDS 33 (Lancet 1998;352:837–853): 3867 people with newly diagnosed T2DM, median age 54 years; over 10 years, median HbA1c 7.0% in the intensive group vs 7.9% in the conventional group; risk of microvascular endpoints 25% lower (95% CI 7–40; p=0.0099), partly due to the need for retinal laser photocoagulation. The macrovascular aggregates in the same study did not decrease significantly. So the statement "control the sugar and myocardial infarction will retreat" does not follow from UKPDS 33. Something else follows from it: early glycaemic work changes the trajectory of the eye, kidney and nerve.
The macrovascular series in people with T2DM often begins before diagnosis. The cluster of insulin resistance, visceral obesity, hypertension and atherogenic dyslipidaemia works for years. Observational data link diabetes to a higher risk of heart failure — in its commentary to the Atlas 11th edition the IDF cites an estimate of "an 84% higher risk of heart failure in people with T2DM than without it". This is an observational association, not a coefficient from a single RCT. An effect on large vessels has been proven not for "diabetes as such" but for specific interventions in specific populations: EMPA-REG OUTCOME — empagliflozin in people with T2DM and established cardiovascular disease; FLOW — semaglutide in people with T2DM and CKD. These trials belong to Module 4; here it is only important not to put an equals sign between "lowered HbA1c" and "lowered major adverse cardiovascular events (MACE: cardiovascular death, non-fatal myocardial infarction, non-fatal stroke)".
One more distinction without which the reading of DCCT breaks. The Diabetes Control and Complications Trial is a type 1 diabetes trial: intensive therapy (mean HbA1c about 7.3%) versus conventional (about 9.1%) reduced microvascular complications by roughly half over 6 years. ADA 2026 cites DCCT/EDIC in introducing the concept of metabolic memory: an early period of near-normal glycaemia leaves a trace in complications even after the groups' HbA1c values have converged. Transferring the "minus 50%" figure to T2DM as is, is a population error. For T2DM the anchors are UKPDS 33 (small vessels) and the caution of ACCORD (large vessels and mortality with an excessively strict target).
ACCORD (Gerstein et al. N Engl J Med. 2008;358:2545–2559. PMID 18539917) randomised 10,251 people with T2DM, mean age 62.2 years, median HbA1c 8.1%, with established cardiovascular disease or additional risk factors. The intensive strategy targeted HbA1c <6.0%, the standard strategy 7.0–7.9%. After one year the medians were 6.4% and 7.5%. The primary endpoint (non-fatal MI, non-fatal stroke, cardiovascular death) did not decrease significantly (HR 0.90; 95% CI 0.78–1.04). All-cause mortality was higher in the intensive group: 257 vs 203 deaths, HR 1.22 (1.01–1.46). The intensive lowering strategy was stopped after a mean of 3.5 years. The population was not "any new T2DM" but middle-aged and older people at high cardiovascular risk. The conclusion for the student: the microvascular benefit of glycaemic control does not license a "the lower the better" target in a frail high-risk person.
The link between resistance and complications is formulated in this lesson as follows. Resistance and hyperinsulinaemia live in the same house as atherogenesis — that is the background of macrovascular risk. Chronic hyperglycaemia glycates basement membrane proteins and triggers the polyol pathway, PKC and inflammation — that is the background of the microvascular series. Treatment that touches only one floor leaves the other.